Sickly Sweet: electronic version

Sickly Sweet: Sugar, Refined Carbohydrate, Addiction and Global Obesity

Simon Thornley and Hayden McRobbie

Simon Thornley and Hayden McRobbieii

Preface

PREFACE

The thesis of this book offers an alternative view of obesity and weight loss. We argue that obesity is a disorder of motivation - an addiction. This distinction is not made just from an academic stand point. The reason we seek to classify obesity in such a manner is to better understand its nature and craft improved strategies for those that are trapped by its snare.

Obesity, at a population level, has not always been with us. Nearly 40 years into the global epidemic, we easily forget that not so long ago the world was not popping its collective buttons. Of all countries, trends in the United States are perhaps most exaggerated. In 1978, 15% of the population was defined as obese, then 22 years later, that number had doubled to 30%, almost one in three adults [1]. Such a rate of change argues that genetic factors are unlikely to account for this trend. If genetic factors are not responsible, the only alternative is the environment. So what is it about our environment that has changed to prompt this global increase in girth? As a medical doctor, during my training, I had been taught the scientific consensus which attempts to explain this modern phenomenon. Succinctly, the World Health Organisation stated that two factors are at work, first, that food has become cheaper and more energy dense, and second, that energy expenditure has reduced, due to a reliance on modern technology, such as motorized transport, which replaces walking or cycling [2]. When examined more carefully, such a view is based on the law of conservation of energy in physics which dictates that energy cannot

iii

disappear from a closed system. In an individual, put simply, energy in must equal energy out. Food intake corresponds to the energy in, and energy expended by the body, carrying out physiological functions, such as pumping blood, maintaining a constant temperature and exercise. If this balance is upset, so that individuals consume more energy than they expend, the excess is stored as fat and obesity results.

At face value, such an argument appears grounded and compelling, based on few assumptions. If such a theory is correct, what is the logical response to reverse this modern epidemic? When nutritional advice is derived from such a theory, of the three main macronutrients (fat, carbohydrate and protein), reduction of proportion of energy derived from fat is the consequence. Why point the finger at fat? When burned, or metabolized, fat releases just over twice the energy of protein or carbohydrate. Co-incidentally, from the 1960s, researchers also recommended reducing intake of saturated fat (mainly derived from animal fat), to prevent the most common cause of death in Western Countries, coronary heart disease. End of story; reducing fat seemed to kill two birds with one stone, potentially reducing obesity and coronary disease in an easily digestible sliver of nutritional advice. The modern epidemic of obesity, so it was believed, would be reversed by skimming fat from milk, trimming the skin off chicken, abstaining from pork crackling and replacing the fat in dairy products with less energy dense carbohydrate.

Unfortunately, population waistlines have not responded in the way predicted by this theory. To the contrary, evidence suggests that such advice has actually increased the prevalence of obesity in most OECD countries, where regular surveys have been carried out. Asian countries in the OECD, of which there are only two, South Korea and Japan, stand out in stark contrast to Western nations, with a stable low prevalence of obesity. The United States, Australia, New Zealand and the United Kingdom, all English speaking nations, stand out in contrast, with the greatest rise in obesity between 1980 and 2003 with prevalence doubling during this period. What is wrong? Two explanations are possible; (1) either people are ignoring this simple health message, or (2) the message is incorrect, or even doing harm.

Preface

The most surprising aspect of this advice is how widely it has been taken up, and how spectacularly it has failed. After the Surgeon General's recommendation in the 1960s that cigarettes cause cancer, many expected that people would heed this advice and leave their cigarettes as soon as the message got through. Fifty years later, one in five New Zealand adults smoke, and although numbers are slowly dropping, progress is disappointing. As far as public acceptance of the crusade against fat goes, it has met with surprisingly little resistance. In New Zealand, chicken is routinely sold, stripped of its fatty flesh, steak is lean, and it's hard to find a can or packet without a reference to it's purity from the obesigenic, greasy substance. Almost all products, from sour cream to biscuits are sold in a “lite” variety, in which fat content is reduced. Where I currently work, in the University’s, School of Population Health, I have no choice but to drink skim milk with my tea or coffee - 99.9% fat free.

My own realisation that traditional nutritional theory may be flawed was initiated by reading Michael Pollan's “In Defense of Food” [3]. Pollan, who describes himself as a humble journalist rather than a scientist, takes on the nutrition establishment, and argues that in the United States, the obsession with healthy eating has paradoxically contributed to obesity. He identifies that food manufacturers have created confusion in the mind of consumers by making claims of health benefits for a wide variety of foods. Also, in the modern food industry's assault on the modern consumer, no one appears to be stating the obvious, straight forward solution to obesity - eat less. Pollan goes on to not only attack nutritional science but also the philosophy of scientific reductionism, arguing that defining food by its building blocks cannot account for its effects on the body. Importantly, also he points the finger at nutritional epidemiology, the science from which nutritional advice springs from, actually suffers from a fundamental flaw. Simply put, individuals are notoriously error prone when it comes to recording what they actually eat, so that measuring associations between food intake and health outcomes may not always produce accurate information on which to base recommendations.

My own experience with food was similar to what I think has been happening on a grand, population wide, scale. During my time as a medical

v


student, I was taught the current medical wisdom. Saturated fat was bad for coronary arteries, and fat in general was obesogenic. I resolved to reduce the fat content of my meals, shunned the weekly regular servings of fish and chips, fast food and resolved to drink only the most watery skim milk. During my time as a clinician, treating people in hospital with heart attacks, strokes and cancer, my approach was the same; fat was the enemy - my patients were encouraged to swap full cream milk for the low fat alternative.

Despite my fat avoidance, belts were loosened and trousers cast aside until I was roughly fifteen kilograms heavier than I had been in medical school. By this time, I was now training in public health medicine, and taking part in research of smokers and how they could be helped to quit. As a doctor in the hospital, I had an almost arrogant disregard for smokers. I hated them. They smoked despite decades of research that showed they were shortening their lives. I'd heard many patients assure me they were going to quit, and later find evidence that they hadn't either from a spouse or from laboratory results. In my mind they were lazy and self-centred, and were responsible for much of the stress I experienced in the over burdened New Zealand public hospital system. As a junior doctor, often exhausted from working long hours, smokers were responsible for what came to them, and that was that.

When I abandoned my career as a hospital doctor, changing instead to public health research, I discovered how little I knew about addiction. For the first time, I realized that smokers experience a withdrawal syndrome when they try to stop, which is unpleasant and lasts for over a month. Symptoms of craving, irritability, restlessness, depression, difficulty concentrating, and constipation plague the smoker bent on reform. These symptoms can get so bad that I've heard of mothers sometimes hitting their children and husbands abusing their wives. Withdrawal symptoms, such as irritability are not a justification for this behavior, but do illustrate the severity of symptoms that some people face. Complete relief is only a cigarette away. Another revelation was the strength of subconscious drives and desires created by reward pathways in the midbrain. Most smokers were completely unaware that the reason they smoked was to avoid

vi

Preface

withdrawal discomfort; the smoking was performed almost automatically. When this was explained to smokers in our studies, instantly the majority agreed and identified personally with this explanation. The last pearl was perhaps the most significant. In almost all addictions, time from taking the substance (such as nicotine from a cigarette) to being absorbed and stimulating the reward centre in the brain was the critical factor that determined how effectively a drug could keep you hooked. Cigarettes were ideal. The nicotine is vaporised by the cigarette's flame, inhaled into the lungs by the smoker, transported rapidly through the heart to the brain in a matter of minutes. The nicotine products (gum, patch, lozenge, mouthspray and pouch) we were testing could not compete. They were absorbed through the lining of the mouth, an area of the body with much less blood flow than the lungs, and their time to stimulation of the brain's reward centres much slower than cigarettes. This time lag had a silver lining, however. Slowly absorbed nicotine helped relieve some withdrawal discomfort, but wasn't as stongly rewarding as the cigarettes they replaced. For many smokers, they are a bridge to freedom.

One day I was working on translating these techniques to help smokers quit into a palatable, brief education session for family doctors. Across the road from where I had lunch was a second hand book store. Among the books that were arranged in a semi-random fashion, I found a couple of cheap copies of old diet books - the New Glucose Revolution, and The Atkins Diet. The book by Robert Atkins grabbed my attention immediately. I knew the diet was based on restricting carbohydrates, out of favour with most nutrition experts, so I was very skeptical. Through the pages, however, I noticed that Atkins described patients who experienced similar feelings to those that smokers reported in cessation clinics. One was very vivid. He described an overweight executive that was addicted to sugar:

‘‘…often I would shake until I could put some sugar in my mouth’’. I had an hour’s drive from my office to my home, and I knew very restaurant, every candy machine and every soft drink dispenser along the whole route.’’

vii


The man experienced tremors that were relieved by a sweet taste, and described his preoccupation with sources of sugar on his journey home. The physical symptoms, relieved by sugar, and the cues described were very similar to the phenomenon of withdrawal described from nicotine. I was curious. I searched medical journals to find evidence that food was addictive, like Atkins’ description, but found little. Much had been written about the theoretical view point, drawing parallels from rat research and from complicated imaging studies of obese people’s brains, but nothing I came across considered the implications of such a theory on how individuals are treated or whether this theory may explain why populations are expanding their collective girth. Also, the fact that I had made such a discovery from a book known to be relegated to the medical scrapheap of pseudoscience increased my cynicism of the established nutritional agenda. Atkins did not identify that these symptoms may have been part of a withdrawal syndrome, but did claim that his diet reduced their intensity and promised recovery.

In the "New Glucose Revolution", I discovered another alternative theory of nutrition and a different approach to weight loss than that advocated by the public health establishment. The most important component was the glycemic index - a physiological measure of how much a standardised mass of carbohydrate from different foods raises the blood glucose after eating. The plots of glycemic index and how it was measured made me think of our nicotine studies and how time-to-‘hit’ was such an important factor in making products addictive. Why couldn't food be considered in the same way? Was glycemic index the key to unlocking a hidden addiction - the obesity epidemic? I was curious to discover more. Together with tobacco researcher, and colleague, Hayden McRobbie, we explore the evidence that links sugar and refined carbohydrates with food addiction and set out an alternative explanation for the burgeoning obesity epidemic.

viii

Preface

REFERENCES

OECD. OECD Health Data 2009: Statistics and Indicators for 30 Countries. Paris: OECD publishing, 2009.

[1]World Health Organisation. Obesity: Preventing and Managing the Global Epidemic. Report on a WHO Consultation Technical Report Series, No 894. Geneva: World Health Organisation, 2000.

[2]Pollan M. In Defense of Food: An Eater’s Manifesto. First Printing. Penguin Press HC; 2008.

ix

Chapter 1

THE GLOBAL OBESITY EPIDEMIC: EPIDEMIOLOGY, HISTORY AND

MILESTONES

“It is not yet clear whether any single attribute of the Western way of life is particularly important in increasing the risk of diabetes. Excess sucrose has largely been exonerated as an important dietary factor in the aetiology of type 2 diabetes...”

J. I. Mann and A. S. Truswell [1]Diseases of overnourished societies and the need for dietary change: in

the Oxford Textbook of Medicine, 4th Edition.

“Originally proposed as the ideal sweetener for people with diabetes... Fructose [part of sucrose]... has been indirectly implicated in the epidemics of obesity and type 2 diabetes.”

The American Heart Association [2]

Sugar and its effect on human health has divided the scientific community over the last ten years. Professor Jim Mann, an international nutritional expert describes sugar (sucrose) as “exonerated” in the aetiology of type 2 diabetes in the prestigious Oxford Textbook of Medicine. The American Heart Association, who, in 2002, had taken a similar view to Mann [1], later changed their mind, reporting that fructose (half of the sucrose molecule) was now facing a guilty verdict, from which it had earlier received a pardon. If one looks back over a longer period of

time, some experts have long scrutinised the adverse effects of sugar consumption, since at least the early 1960s [3]. Such calls, however, have largely been ignored until recently. In this book, we examine what direction nutritional policy has taken over the last forty years, and in what nutrition context obesity patterns have developed. We examine overeating from a new paradigm, rather than viewing overeating as a problem of energy balance, we instead consider motivation to eat, and what effects different foods have on hunger. Surely, if eating certain types of food, increases appetite, as alleged for sugar, this has important consequences for the quantity of food that enters a person’s mouth, ultimately stretching the belt out a notch, and making difficult work of the juxtaposing of buttons. We will see that such a paradigm, ignoring the powerful biological drives and learning that occur with eating, has lead to what we believe to be a tragic misdirection of nutrition policy in English speaking countries and now dispersing around the world.

When I first started work as a house officer, fresh out of medical school, at the dawn of the new millenium, I spent two years working in a busy city hospital. The hospital treated people of a wide variety of ethnic backgrounds, but Pacific people had a lively community in the area and were frequently in need of treatment. Migrants from the Pacific islands that surround New Zealand are frequently obese, so much so, that during my public health training, a colleague advised me that one in four Pacific adults would be eligible for obesity surgery in the jurisdiction in which he worked. Of all the challenges that being a junior doctor entailed, one of the most difficult tasks was the constant need to place intravenous lines in patients, so that various drugs, and fluids could be administered. What, in a thin person, was a trivial task, could provoke severe anxiety when veins were concealed by layers of fat. If requested to insert a cannula, I would first take a peek through the curtain to get a rough estimate of how much fat was likely to impede my progress, and so how many spare lines would be required. In people who tipped the scales, I would load my kidney dish of supplies to overflowing to account for the inevitable event of numerous embarrassing and painful (for both the patient and myself) failures. Once established in the job, I soon realised that the sneak preview was

The Global Obesity Epidemic

unnecessary, because the vast majority of people admitted were overweight. I might as well overload my kidney dish, the chances were I'd have a battle on my hands. Faced with the relentless demands of caring with such a load of obese patients, it was difficult to imagine a time when obesity was a rare sight.

For anyone in an English speaking country, obesity has become such a common occurrence it no longer raises more than a glimmer of curiosity. TV, voyeuristically, still portray the adventures of the super obese, that continue to pull crowds. Only grossly or morbidly obese people attract comment. Indeed, whilst writing this manuscript, the researcher sitting adjacent to me would easily qualify as obese. Although records are rare, before the 1970s, few Western countries systematically recorded obesity rates in their populations. Why no scientific interest in body size? It seems that excess fat simply wasn't a major issue to devote significant time or resource to measuring. This, in itself, suggests that obesity was not a major concern - why measure a problem that doesn't exist?

Something changed in the 1970s. From the early 1980s, obesity suddenly appeared on the public health radar, and populations, particularly in wealthier countries, were measured for height and weight. The expanding waistlines of different countries have been thoroughly researched, documented up until today, with collective expansion set to continue for the foreseeable future. This bleak news hides pockets of resistance to this trend. Despite this pessimistic outlook, some countries remain thin. Obesity is strongly patterned by country. Of the thirty wealthy countries contained within the Organisation for Economic Co-operation and Development (OECD), English speaking countries are leading the pack, with the United States way out in front [4]. In sharp relief to these countries that are linguistically linked, are the slim societies of Japan and South Korea who have maintained low levels of obesity over the same period.

To understand what factors underlie the rising tide of global obesity, a phenomenon with a clear temporal pattern, with vastly different impacts between countries, we must consider what ideas have been propagated in these countries, what dietary patterns have emerged and consider

3


definitions of obesity. Critical milestones, in terms of nutritional advice, and changes to food processing and content may give clues to what is causing our collective bursting of buttons.

DEFINITIONS

Firstly, how do we define someone as overweight or obese? This sounds simple, but accurate, repeatable, consistent measurements are critical to our understanding of this disorder. Body mass index (BMI) is commonly used as a global standard today to define obesity in terms of weight corrected for height [5]. What is this measure and what does it tell us about an individual? How has this definition changed over time, and what does the commonly used term “body mass index” indicate? Obesity has been labeled a major public health issue because of its association with premature death and other diseases. If information is to be accurately recorded, a consistent definition must be applied over time to track population trends. Before 1980, a variety of methods were used to classify people as overweight, based on actuarial data derived from life insurance companies such as Metropolitan Life, which were labeled “ideal” weight for height values, or “desirable” body weights [5]. Such standards were derived from a large group of North Americans and Canadian adults purchasing life insurance policies between 1935 and 1954, with standards referring to a group of people that, at the time, had low rates of premature death. From 1980, body mass index (BMI) was more commonly used, which is defined by weight in kilograms, divided by height in meters squared. This measure is a reasonably good measure of body fat, although it is far from perfect. Raised BMI also predicts increased risk of a range of diseases such as coronary heart disease, stroke, cancers of the large bowel, womb and breast [6]. A recent study, involving over 900,000 subjects, showed that a body mass index of 22.5 to 25.0 kg/m2 was linked with optimal survival. People above this range, with moderate obesity (BMI between 30 and 35 kg/m2) would, on average, face in excess of three years life lost, and people with extreme obesity (BMI 40-50 kg/m2) lost more

4


than 10 years of life. By way of comparison, this latter condition shortens average lifespan by about the period as a lifetime of smoking cigarettes [7]. Classifications based on body mass index are therefore usually divided into overweight (BMI ≥ 25.0), and obese (BMI ≥ 30.0).

While BMI is a useful measure for characterizing population risk of obesity, at an individual level it may be less accurate because some, particularly young males, are incorrectly misclassified as overweight due to increased lean muscle mass rather than excess fat tissue. To avoid this potential source of error, here, we use a cutoff of BMI ≥ 30.0 kg/m 2 to classify individuals as obese, and to monitor population trends.

5


Figure 1. Adult obesity (BMI ≥ 30kg/m2) prevalence by year for selected OECD countries (1980 to 2003) [9].

GLOBAL TRENDS IN OBESITY PREVALENCE

The start of the global obesity epidemic is difficult to pinpoint. Regular, representative surveys of population obesity were not carried out until obesity became a focal point in the medical community and significant resource was devoted to its measurement. In the United States, at the turn of the 19th Century, a survey was undertaken, recording height and weight of Civil War veterans aged 50 to 59 years found that 3.4% had a BMI ≥ 30.0 (obese) [16]. Also, a comparison of the weight of London

6


hospital patients coming to autopsy in 1906 to 1914 and the 1950s showed little difference in mean weights between the two periods [8]. Since this time, until the early 1980s, nationwide, estimates of obesity prevalence are difficult to find. A summary of obesity prevalence, by country, has been published by the OECD and the prevalence by country between 1980 and 2003 are depicted in Figure 1.

Several patterns emerge from this figure. First, the country with the highest prevalence, reported after the year 2000, of obesity is the United States, with one in three adults meeting the BMI cutoff. Other high prevalence countries are also English speaking, with New Zealand and the United Kingdom (one in four) and Australia (one in five) next highest. These within-country trends hide patterns present in some ethnic groups. For example, 43% of Maori and 65% of Pacific adults are obese [10]. Also, the rate of change of obesity (slope of the line) is highest in these English speaking countries (Canada excepted). Further, Japan and South Korea (not displayed) have the lowest prevalence of obesity, of all countries in the OECD, with fewer than one in twenty adults falling into this category. Other continental European countries, along with Ireland, occupy the middle ground between English speaking and Asian nations. What conclusions can be drawn from this information? First, we observe that obesity prevalence is slowly rising in all OECD countries presented here, so that an increased burden of obesity is a real global phenomenon. Also, different rates of change in obesity prevalence are observed between countries with similar cultural and linguistic traditions. What is it about English speaking countries that caused obesity rates to climb so steeply in the latter part of the twentieth century? To answer this question, we will consider what changes in nutrition have occurred in these countries.

NUTRITIONAL CHANGE BEFORE THE 20TH CENTURY

Although record keeping before the 20th century was not as comprehensive as today, historians of coronary disease have attempted to document what nutritional changes predated the epidemic of

7


cardiovascular disease observed in the 1950s. Michaels [11] documents that sugar consumption only became established in Europe in the 16 th

century, after mass cultivation of sugar cane got under way in the West Indies. With the advent of tea and coffee drinking in the 18 th century, sugar became more popular. Intake of sugar increased in Great Britain from about 2kg/capita/year in 1700, to 9.5 in 1809-13, increasing to 50.6 in 1962. In contrast, Michaels identifies that an historic author King, who in 1696 provided an account of all aspects of English life, estimated that consumption of meat was about 37kg/year. King estimated that half the population (about 2,700,000 people) ate flesh regularly and their consumption was about 3.6kg/capita/year higher than people in the UK in 1962. Thus total animal fat consumption had probably decreased rather than increased over this critical period. In contrast, average sugar intake has continued to rise [14].

CHANGES IN NUTRITIONAL SCIENCE DURING THE 20TH CENTURY

Concern about obesity did not preoccupy nutritionists and the medical community during the early part of the 20th century. Before obesity ever appeared as a public health issue, blocked coronary arteries from fatty deposits, causing an epidemic of heart attacks and premature death were the primary motivating force behind public health campaigns to change what the public consumed [13]. Despite the fact that coronary heart disease, known more commonly as heart attacks and angina, is the most common cause of premature death in most developed countries, this was not always the case. It wasn’t until mid way through the twentieth century that coronary artery disease was commonly encountered in clinical practice.

The first hint of coronary artery disease was recorded in 1768, when the famous Physician, William Herbeden described angina pectoris, which was the sensation of being strangled in the chest [11]. At the time, he did not make the connection between these symptoms and the heart. Historical evidence suggests that although the condition was first described at this time, it was still extremely rare. Hebeden himself records only

8


encountering 20 cases of angina during his twenty or so years of practice. Records indicate that cases were extremely rare from the late 18 th century until 1912, when Herrick described a series of six cases with coronary thrombosis, a blood clot in the arteries supplying blood to the heart muscle. This anatomical basis for these symptoms was discovered 32 years earlier by Weigert. Even in the early 20th century, death from coronary disease was a rare event. Michaels reports evidence that deaths from hardening of the arteries (arteriosclerosis) were 200 times more numerous in 1962 as 1901-10. A common objection to such evidence of a rapid rise in the number of cases of coronary artery disease, was that life expectancy was increasing, and that latter populations were much older, and thus more likely to develop disease. Although the number of people aged 50 years or older did increase in the UK over this period, the magnitude was much smaller (threefold; 4,790,000 in 1901 to 14,158,000 in the early 60s) than that observed for increasing rates of disease [11].

By the early 1960s, however, the epidemic of coronary artery disease was established in Western industrialized nations, and doctors and scientists were seeking explanations. Figure 2 shows the rapid rise in mortality rate from coronary disease and stroke in England and Wales between 1921 and 1939 when the epidemic was first identified in medical journals, in 1949.

9


Figure 2. Comparative mortality index for different causes of death in males in England and Wales between 1921 and 1939 [12].

The medical, public health and epidemiological communities swung into action to prevent the rapid rise in cases of coronary disease. Gary Taubes, a science writer, has documented the history of nutritional recommendations associated with the diet-heart-hypothesis, developed in the 1930s, and widely accepted in the early 1980s, lead by Dr Ancell Keys [13]. He documents that the American Heart Association released a report in December 1960, arguing that “the best scientific evidence of the time” strongly suggested that Americans would reduce their risk of heart disease if they reduced the fat in their diet and replaced saturated or animal fat with vegetable-derived fat. Initially the advice was aimed only at men at high risk of heart attacks by virtue of having suffered a previous event, having a high cholesterol or being smokers of cigarettes. Such recommendations were revised annually, so that in 1970 the advice applied to all Americans (including infants, children, adolescents, pregnant and lactating women and older people). ‘Eat less fat’ was the mantra that we were both taught at medical school, as the answer to both obesity and coronary heart disease.

10


Keys believed that the ideal heart healthy diet would increase the percentage of carbohydrates from less than 50% calories to 70%, and reduce saturated fat consumption from 40% to 15%. In contrast, Taubes notes that Japanese physicians were advising patients to increase their total cholesterol levels, because low cholesterol levels were associated with risk of haemorrhagic stroke in their home country.

Barry Popkin, a Professor of Economics, has described changes in the North American diet and contrasted these with changes in Korean and Japanese diets in the latter half of the twentieth century [14]. His analysis is based on population estimates of food consumption derived from United Nations Food and Agriculture Organisation Food Balance Sheets. Per capita consumption of a range of food products was estimated by calculating the national total of food-stuff produced, adding imports and subtracting exports, then dividing the difference by the total population estimate at that point in time. The remainder is considered to have disappeared and so assumed eaten, although a small amount is likely to be wasted. Popkin’s findings showed that, in the United States, the key changes that occurred between 1977-8 and 1987-8 were a reduction in whole milk consumption (50 gram/capita/day) with a compensatory increase in low fat milk (30 gram/capita/day), along with a decline in high and medium fat red meats (30 gram/capita/day), and an increase in low fat poultry consumption (10 gram/capita/day). Conversely, soft drink consumption increased markedly, with an increase in sugar sweetened soft drinks of 60 gram/capita/day, and diet drinks by 45 gram/capita/day over this ten year period. In line with the American Heart Association’s guidelines, this analysis, suggests that fat consumption was reduced, with a large increase in carbohydrate intake, particularly from sugar sweetened soft drinks. Like the United States, the National Heart Foundation in New Zealand, Australia and the United Kingdom have consistently advocated for reduced consumption of dairy fat, meat fat and reduced fried food intake.

Asian countries, present in the OECD obesity analysis, have undergone paradoxical changes to those observed in the United States. Although overall fat intake is much lower in these two countries than the US, per

11


capita fat consumption increased 341 percent between 1946 and 1987. In South Korea a similar trend has occurred, with a rising consumption of animal products and declining intake of grains during the period between 1965 and 1985. Percent of energy derived from fat rose from 8% to 14%, and similarly average grain consumption reduced from 550 to 400 grams/capita/day during this twenty year period. Combining such data with the trends observed in obesity over the last thirty years (Figure 1), we observe that this increase has not had a substantial impact on the prevalence of obesity in Japan, or South Korea (data not shown), although the prevalence of people who are overweight elsewhere has grown substantially in recent decades.

So, we have seen a clear difference in the body composition of selected countries, in which records of body size, and per capita intake of energy have been recorded. A clear distinction can be drawn between countries who have experienced a rapid increase in the proportion of obesity people over the last thirty years – USA, Canada, UK, Australia and New Zealand; and those countries that haven’t – Japan and Korea.

SUMMARY

What conclusions can we draw from these historical events? First, coronary artery disease is a relatively recent phenomenon, and it was this epidemic which prompted calls from medical authorities to lower fat intake, particularly in English speaking countries. Second, sugar consumption has substantially increased over the last three hundred years, and calls to reduce fat intake, by public health authorities, may have increased the consumption of carbohydrate and sugar in countries with a British colonial heritage. Conversely, in Asian countries, which were rising out of poverty during the 20th century, fat was more commonly consumed that ever. With two quite different changes in nutrient profile, the change in obesity prevalence between Asian countries and English speaking countries, recorded from the early 1980s, couldn’t be more different. South Korea and Japan have maintained very low levels of obesity in the last

12


thirty years, despite a dramatic increase in the proportion of calories obtained from fat. In the remaining chapters we explore the health effects of carbohydrates, the macronutrient promoted to prevent coronary artery disease in English speaking countries during the early 1970s, initiated by the American Heart Association. We also research the effect that carbohydrates have on the motivation and reward centres of the brain. Has the advice, to reduce fat, and saturated fat, been a case of robbing Peter to pay Paul? For us to consider whether the growth in global obesity has occurred due to carbohydrate addiction we will have to consider what has is known about addiction, and carbohydrates. First, we attempt to unpack the concept of addiction. How do we know something is addictive? What has been learned about treating people with addictions? Could this information help us, collectively, beat the obesity epidemic?

Figure 2. Changes in consumption of selected food types, 1969 to 1985 [15].

13


REFERENCES

[1] Mann, JI, Trusswell, A. S. Diseases of overnourished societies and the need for dietary change. USA: Oxford University Press; 2003.

[2] Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig RH, et al. Dietary Sugars Intake and Cardiovascular Health: A Scientific Statement From the American Heart Association. Circulation. 2009;120(11):1011-1020.

[3] Yudkin J. Dietary fat and dietary sugar in relation to ischaemic heart-disease and diabetes. Lancet. 1964 Jul 4;2(7349):4-5.

[4] OECD. OECD Health Data 2009: Statistics and Indicators for 30 Countries. OECD publishing; 2009.

[5] Kuczmarski RJ, Flegal KM. Criteria for definition of overweight in transition: background and recommendations for the United States. Am J Clin Nutr. 2000;72(5):1074-1081.

[6] Prospective Studies C, Whitlock G, Lewington S, Sherliker P, Clarke R, Emberson J, et al. Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies. Lancet. 2009;373(9669):1083-96.

[7] Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. BMJ. 2004 Jun 26;328(7455):1519.

[8] Morris JN. Recent history of coronary disease. Lancet. 1951;1:1. [9] OECD. OECD Health Data 2009: Statistics and Indicators for 30

Countries. OECD publishing; 2009. [10] Ministry of Health. A Portrait of Health: Key Results of the 2006/07

New Zealand Health Survey. Ministry of Health; 2008. [11] Michaels L. Aetiology of coronary heart disease: an historical

approach. British Heart Journal. 1966;28:258-64. [12] Ryle JA, Russell WT. The natural history of coronary disease a

clinical and epidemiological study. British Heart Journal. 1949;11(4):370-389.

[13] Taubes G. The Diet Delusion. New York: Vermilion; 2007.

14


[14] Popkin BM. Nutritional Patterns and Transitions. Population and Development Review. 1993;19(1):138-157.

[15] Kim SH. Changing nutritional status affected by rapid economic growth of Korea. In: International Symposium on Food Nutrition and Social Economic Development. Beijing: Chinese Academy of Preventive Medicine; 1991. p. 472-478.

[16] Helmchen LA, Henderson RM. Changes in the distribution of body mass index of white US men, 1890-2000. Annals of Human Biology. 2004;31(2):174-181.

15

Chapter 2

ADDICTION: CLINICAL FEATURES AND BIOLOGY

After first reporting global trends in food and nutrient intake, then recent trends in obesity, you may wonder why we are now venturing into seemingly unrelated territory. To the contrary, we believe that recent global food trends may only be understood by considering the rewarding properties of food, and the similarities between these everyday items and

other products commonly accorded ‘addictive’ status. Of course many of

the substances we frequently refer to as addictive are often illicit, or their supply is controlled in some way. Cigarettes and alcohol are common suspects, leading to addiction, but food, surely not - we retain conscious control of what we eat for breakfast, lunch, dinner and in between, don't we? Does eating share characteristics of addictions more commonly seen with drugs? Before we can answer this question, we must consider what features make a drug (or food) addictive? How is addiction recognised? Which techniques can help people beat addictions? We discuss the general features of addiction, so that we can make sense of eating behavior and obesity – do they fit the same mould?

Many medical professionals would strongly refute the hypothesis that some foods (such as sugar) have ‘addictive’ properties. What we propose here goes against the grain. This is, however, often how the medical field develops. Take nicotine for example. Today, people generally agree that

nicotine, present in a cigarette, is responsible for hooking people on tobacco. However this was not always the accepted mantra. Not until the 1970s was nicotine first recognised as a drug of dependence. Before this, most scientific bodies viewed smoking as a habit, not an addiction. The rationale of this thinking, at this time, was that a well-defined withdrawal syndrome after stopping smoking was not well described and methods available were equally effective, or ineffective for helping people stop for good. Sound familiar? In 1971, Russell, a pioneer in the study of tobacco, published an argument that nicotine was a dependence-producing (addictive) substance [1]. This was the beginning of a change in attitudes towards smoking. Soon after, the Royal College of Physicians decreed that tobacco smoking was due to nicotine addiction and in 1980 the American Psychiatric Association (APA) recognised that smoking met most of the criteria for drug dependence, so that this condition was then included in their diagnostic “bible”, the DSM-III. It was not until the late 1980s that the US Surgeon General issued a report entitled ‘Nicotine Addiction’, which concluded that tobacco was addictive, nicotine was responsible, and that the effects of nicotine on the brain share features of other major drugs of addiction such as heroin and cocaine [2].

WHAT IS ADDICTION?

To lay people, the word 'addiction' conjures an image of a sad alcoholic or cocaine addict, lost in their own world, often dishevelled, caring for nothing else but another fix from their drug of choice. Other less intense preferences for substances are more commonly referred to as habits, implying that they are easier to give up. The chances are, whether, working as a health care professional or not, most of us can picture a person who roughly fits the addiction stereotype. Although, at first glance, this may sound simplistic, it reveals two key components of addiction, the substance and the individual’s relationship with it. In the familiar case of substance abuse to cocaine, or alcohol, the primary place in the person's life that the substance takes, distinguishes the addict from those around

Addiction: Clinical Features and Biology

them. While others may place no value on acquiring or consuming the substance, to the addict, their object of desire dominates their priorities and they have difficulty controlling their use of it. Time is spent ensuring that the addict has sufficient supplies, usually to avoid the unpleasant feelings of withdrawal that might accompany prolonged abstinence. Time spent obtaining the substance often takes precedence over other priorities, which might be thought, on considered reflection, to be more important: such as family, work and the wider community. Medics are generally well versed in these consequences, with a mnemonic summarising the most commonly harmed areas of a person's life: health (liver), family (lover), work (livelihood), and society (law).

Such extremes allow us to falsely assume that addiction, and the processes that underlie it, only occur in a small subset of the population. Addiction can, however, be more subtle and resist these stereotypes. For example, perhaps the most common daily addiction is caffeine. Although, coffee and tea drinkers’ lives are usually not ruled by their caffeine intake, some characteristics of more severe addiction syndromes are shared. For example, the presence of a withdrawal syndrome is closely tied to addiction and substance abuse. Caffeine withdrawal is a subtle discomfort that starts soon after abstinence. Although the symptoms would be unlikely to ever prompt a visit to the doctor, they are nonetheless real. Cravings and urges for a source of caffeine, headaches, reduced concentration, irritability and restlessness are an attempt to more accurately label the feeling of “not quite feeling right”. Regular tea and coffee drinkers rarely, if ever, have to remind themselves of their need for a cup. Often the smell or sight of the substance will initiate the caffeine addict to reach for the tea bag or plunger.

Although we may not realize it, our brains are hard-wired for reward. We need to eat, drink and reproduce to survive so that behaviours associated with such necessities are rewarded. The ‘machinery’ that is responsibly for subconscious reward lies in a part of our brain that governs automatic survival functions. It’s known as the mesolimbic dopaminergic pathway and consists of a number of structures in the midbrain and prefrontal cortex. Activation of this brain pathway leads to reward,

19


subconscious learning and the feeling of pleasure. Food, for example, stimulates this pathway which ultimately leads to release of the chemical messenger, dopamine, and a sense of pleasure. However the ‘amount’ of pleasure depends on how enjoyable the food is and how hungry you are at the time of eating [3]. It just so happens that drugs such as nicotine and cocaine hijack this reward system and, depending on our genetic makeup, the environment in which we live, and our backgrounds, some people are more susceptible than others.

The mechanics of what motivates an addict are often glossed over unless one pays careful attention to the subtle symptoms that precede substance use, and observe what effect use has on such symptoms. Let’s go back to our example of nicotine. Unlike cocaine and heroin, a puff on a cigarette does not give you much of a ‘positive hit’. For those who have ever tried smoking, you will, no doubt, remember your first few puffs. I doubt that it left you feeling high and wanting more. In fact you probably felt a bit sick. With persistence, however, smokers develop tolerance to these unpleasant effects. One might think then that because nicotine is only a mild stimulant, it might be easier to give up than other drugs of dependence, such as alcohol, cocaine or heroin. This, however, is not the case. Early studies that investigated the ‘addictiveness’ of nicotine asked people who used tobacco, cocaine, heroin and alcohol to rate how much they liked each drug (on a 5-point scale: 1=dislike; 5=like a lot) and how much they needed to use each drug (on a 4-point scale: 1=no need; 5=need a lot). Tobacco rated second for ‘liking’, after heroin, and in terms of ‘needing’, tobacco came out on top, followed by heroin, cocaine and alcohol [4]. These results showed that most smokers do not smoke tobacco for the positive effects but instead to keep themselves from withdrawal. The onset of subtle withdrawal symptoms that follow abstinence become increasingly unpleasant until relief is sought. Drinking a cup of coffee, injecting or snorting cocaine, or smoking a cigarette deliver variable amounts of euphoria, but they all consistently relieve negative withdrawal symptoms in their respective addicts. This sense of relief becomes a subtle but powerful motivator – more so than the ‘hit’. Familiar learning mechanisms consist of the reward that accompanies good behavior, or

20


positive re-inforcement. For example, children receive praise from their parents for good behavior to increase the chance that the child continues to behave in the future. More subtle is the converse when feelings of discomfort or pain are relieved. For example, the relief one gets from removing tight shoes, or a heavy load. Such relief is often experienced as pleasure, and can be indistinguishable from positive reward when unpleasant effects are regular and sustained. This mechanism, called “negative reinforcement” is a powerful motivator. We have glossed over some of the important features of addiction, but how has addiction been traditionally defined within medical and psychiatric circles?

DEFINITIONS

Various authors or professional bodies have attempted to define addiction, although wide variation exists and agreement about the precise meaning of the term lacks consensus. Perhaps the best known definition of addiction, often used in clinical practice, is the Diagnostic and Statistical Manual (IV), published by the American Psychiatric Association [5]. To fulfill the criteria, the patient must recount at least three or more of the following over a twelve month period:

1. Taking larger amounts and over a longer period of time than was intended

2. Unsuccessful efforts to cut down or control substance use3. Overinvestment of time spent in activities to both obtain and use

the substance, or recover from its effects4. Giving up important social activities to use the substance5. Continued use despite negative consequences, such as health risks6. Tolerance - having to use more of the substance to achieve the

desired effect7. A withdrawal syndrome that occurs after periods of abstinence; or

the substance is used to avoid such symptoms.

21


This definition embodies the three most important elements of addiction - the failure of resolve to reduce consumption in the face of negative consequences, along with the physical dependence elements of symptoms of withdrawal and tolerance.

The International Classification of Disease was developed by the World Health Organisation in the late 1800s to systematically classify disease [6]. The most current version (ICD-10) defines substance dependence similarly to the DSM. The ICD-10 requires a minimum of three criteria to be met for a person to be considered dependent. These include: (1) a strong desire or compulsion to take the substance; (2) difficulties controlling substance-taking behaviour; (3) a withdrawal syndrome that becomes evident when substance use is stopped; (4) tolerance; (5) neglect of other pleasures or interests in life; (6) continued substance use despite knowledge of harm; and (7) the person should either use, or have a desire to use the substance.

The DSM IV criteria for substance abuse only apply to illicit substances such as opiates (cocaine or heroine), or amphetamines, and have some limitations. Let’s compare heroin and nicotine use. Heroin fulfills all criteria with ease. Nicotine use fits with the withdrawal criteria, difficulty controlling use or compulsive use, and use despite the occurrence of related harm. The remaining four criteria, however: tolerance, using more than intended, spending a great deal of time using the drug and giving up activities to use the drug, don’t as easily apply. These differences are not solely due to the nature of the addiction to these substances, but also relate to the social context. If use of these substances results in breaking the law, and isolated social circles; then the deterioration in social function as a result of these disorders can vary widely. For example, before opiates were criminalised, several famous authors, such as Thomas de Quincey and Samuel Taylor Coleridge used heroin daily, yet still published influential works of prose during this time, and participated in society without scorn or isolation. Caffeine use also does not, as far as we know, cause harm to health, however, a withdrawal syndrome and tolerance to the substance is commonly reported. Caffeine addicts (us included) can carry out normal social and work functions, even with frequent need for drug

22


use. If caffeine were suddenly criminalized we would be in trouble! Caffeine illustrates one important feature of addiction – that addictive substances are not necessarily harmful to health. The same is true for nicotine. If smokers didn’t inhale the tar present in cigarettes, they wouldn’t suffer any adverse effects, as far as we know. Nicotine, taken in isolation, such as through patches or gum, has little or no adverse effects on health.

Although addiction is most commonly described in association with substance use, other addictions have been described for behaviors that do not involve substances at all. Examples include gambling, sex, and internet use.

Delving deeper into the machinery of addiction, an important element, not captured in official definitions, is the value the addict places on immediate over delayed rewards. Ainsley [7] noted that a pervasive element of the learning in animal and human subjects is the high value placed on small, but immediate rewards over delayed, larger ones. Although such preferences are observed in normal people, people with addictions have an even stronger preference for rapid gratification. Such a preference is reflected in the rate of absorption of drugs of abuse. Drugs or substances with the greatest addictive potential tend to be quickly absorbed, so that time to relief of withdrawal symptoms is short. These characteristics may be manipulated to help people with addiction recover. Perhaps some of the best known drugs which assist recovery are nicotine replacement therapy, in the form of gum, transdermal patch, or lozenge. Cigarette smoke is inhaled, and absorbed across the small air sacks (alveoli) in the lung. The high rate of blood flow through the lungs, coupled with the vast surface area of the alveoli, result in rapid absorption of the nicotine and rapid relief of tobacco withdrawal. What seems, on paper, to be a favourable effect of the drug, also gives the product its addictive sting. Cigarette companies manipulate the pH of tobacco smoke, by adding ammonia to increase its rate of absorption and thus the addictive potential of their products. In contrast, nicotine gum, for example, releases nicotine slowly after chewing, across the lining of the mouth. The lower blood flow and lower surface area of this body region, slow the absorption

23


of nicotine. As a result, nicotine gum more slowly relieves tobacco withdrawal discomfort, but is much less likely than cigarettes to be used long term. In a similar manner, methadone is often used as a bridge to recovery for users of intravenous opiates, such as heroin. We will consider in later chapters how this important concept may be applied to food. If obese people are addicted to some foods, giving the food version of the nicotine patch, may provide a path to recovery.

CLINICAL FEATURES OF WITHDRAWAL SYNDROMES

Although we have briefly discussed the salient features of addiction, we will discuss further the nature and time course of common withdrawal symptoms in more detail. A wide variety of symptoms are described after abstinence from different substances, and some are better known than others (Table 1). The presence of withdrawal symptoms is often considered a pathognomonic, or unique, sign that a substance should be considered addictive [8].

Of commonly encountered withdrawal syndromes, perhaps that associated with alcohol withdrawal is best known. Classic symptoms have been described since antiquity, and are best known as delirium tremens. The symptoms are often so severe, that patients abstaining from alcohol after a heavy drinking career are frequently treated in a specialised unit to recover. In the first three days after stopping alcohol, patients often develop psychiatric symptoms in which they percieve their skin to be crawling with ants or other insects. They also have dramatic fluctuations of physiological measures such as heart rate, blood pressure or temperature. These symptoms are often treated with drugs such as benzodiazepines, if available. After about ten days, such dramatic symptoms subside, but urges and cravings to drink continue. The most severe symptoms last for about three months, then slowly resolve. Despite the resolution of these withdrawal symptoms, recovered alcoholics are often aware that no more than a single drink of alcohol can undo months of recovery, and send them back down a destructive path.

24


Table 1. Signs and symptoms of nicotine and other substance withdrawal

Alcohol

Opioids Sedatives

Cocaine

Nicotine Stimulants

Sweating Yes YesNausea Yes Yes YesChange in heart rate

Increase

Increase Decrease

Sleep Disturbance

Yes Yes Yes Yes Yes Yes

Anxiety Yes YesDysphoric mood

Yes Yes

Fever YesIncreased appetite

Yes Yes

Irritability Yes YesDifficulty concentrating

Yes

Time courseOnset 6-12

hours4-6 hours

1 week 2-12 hours

Peak 3-7 days

2-3 days 2-3 days

Duration 1-2 weeks

2 weeks Up to 10 weeks

3-4 weeks

Adapted from: American Psychiatric Association 2000; Hughes et al. 1994.

25


Tobacco withdrawal symptoms are more subtle than those observed for alcohol, but retain considerable hold over recovering smokers. Symptoms include:

1. Craving and urge to smoke2. Increased appetite3. Reduced concentration4. Restlessness5. Depressed mood6. Constipation7. Mouth ulcers (less common) [9].

The severity of tobacco withdrawal is generally less than that associated with opioid or alcohol withdrawal and may have a lesser effect on the ability of an addict to undertake normal daily activities. Just because the tobacco withdrawal syndrome may be less severe it does not mean that it is easier to quit than other substances. For example Kozlowski [10] surveyed 1000 people seeking treatment for drug or alcohol dependence and asked them how difficult quitting smoking cigarettes would be compared to stopping other substances. Over half said that cigarettes would be harder to quit, even though they rated cigarettes as less pleasurable to use.

Although the nature and severity of these symptoms varies substantially between patients and different substances, the time course over which the withdrawal symptoms occur is relatively constant. If the smoker is able to hold their resolve and abstain continuously, the severity of symptoms generally peaks in the first three days, then wanes over one to three months. A similar time course is observed with opiate, alcohol, and metamphetamine addiction. Abstinence is tenuous in people with addictions, partly from the knowledge, often subconscious and deeply ingrained, that relief from these unpleasant symptoms is only one smoke, snort or drink away. The sight of other users acts as a cue, amplifying urges, cravings and desires to consume the addict’s substance of choice. While these withdrawal symptoms may respond to the effects of slow

26


release forms of the addictive substance, this treatment often only partially relieves such unpleasant symptoms, often not giving the same 'hit' as the addictive substance.

BIOLOGICAL BASIS OF ADDICTION SYMPTOMS

Although we don’t delve too deeply into the technical detail, we will briefly touch on how neuroscience has added a further dimension to our understanding of addiction, outside the clinical picture, previously described. The identification of the part of the brain activated by drugs of abuse has contributed to our understanding of what makes some substances addictive over others. The origin of addiction has been linked to a part of the human brain responsible for subconscious control of behaviour and motivation, associated with survival functions, such as eating, drinking and sexual reproduction. One can readily appreciate that drug addiction may be viewed as a ‘hunger’ for drugs, such that some substances become as important, or even more important than eating food and consuming water and other drinks. This anatomic site, the dopaminergic mesocorticolimbic projection or reward centre, present in the midbrain, is most often implicated in the biology of addiction. In human and animal studies, administration of substances of abuse increases concentrations of the chemical messenger or neurotransmitter, dopamine, in this centre, considered the main component of the brain reward system [11]. For example, an intravenous dose of cocaine results in increased release of dopamine by blocking re-uptake by nerve terminals in a part of the brain called the nucleus accumbens. Other substances, such as opioids, nicotine and alcohol act in a different area of the reward pathway, stimulating nerve cells in other regions, which ultimately influence the nucleus accumbens, increasing dopamine concentrations in this area. This common anatomic site, along with the linked chemical, dopamine, has therefore, progressed our understanding of the biology of drug addiction, and their common features [12].

27


What are the clinical features of drug-induced dopamine release in human subjects? Two principal effects are commonly described [12]. Firstly, release is accompanied by pleasure, or the feeling of a ‘hit’ and behaviours that produce this are reinforced. A vicious cycle results in deep seated learning to take the substance. The increase in dopamine concentration focuses the individual on sensory elements (‘cues’, such as the smell of tobacco among smokers) associated with drug taking. The sensation of such elements often initiates automatic, subconscious, Pavlovian stimulus-response drug taking when an individual is subsequently exposed to these cues. This is commonly observed in people that smoke, so that the sight of cigarettes, other people smoking, ash trays, or lighters, can ‘switch-on’ the automatic lighting of a cigarette, in people addicted to tobacco [13, 14].

Although dopamine has been closely linked to addiction, the neurotransmitter also plays a role in people with psychosis – seeing or hearing things that are not there. Indeed, dopamine has been referred to as the “wind of the psychotic fire”, when describing its pivotal role in the symptoms and treatment of psychotic disorders such as schizophrenia [15]. Evidence for dopamine's importance emerges from clinical practice - for example, treatment of patients with Parkinson’s disease using therapeutic doses of levo-dopa, a dopamine like substance, can result in a drug-induced psychosis in a small proportion of these patients. Conversely, drugs used to treat psychoses such as schizophrenia interfere with dopamine pathways, and may result in unwanted Parkinsonism, manifested by expressionless, blank faces and a characteristic pill-rolling tremor.

If addiction and psychosis share the same biological pathway and neurotransmitter (dopamine), then we might expect that such mental disorders and addiction commonly coexist in individuals. For workers in the mental health field, such disorders are all too frequently associated, with the term “dual-diagnosis” used to summarise the occurrence of the two disorders in the same patient. In one summary, the prevalence of smoking was between 80 and 90% in people treated in hospital with schizophrenia [16]. Numerous epidemiological studies describe the co-occurrence of schizophrenia and other forms of addiction, such as to

28


alcohol, metamphetamine and opiates [16]. Further, the presence of illicit drug use in people with schizophrenia predicts relapse, treatment resistance and need for further hospital treatment.

Logically, we might expect that if obesity and weight gain are also related to this pleasure chemical, dopamine, then when the effects of dopamine are blocked in some way, for example by drugs that exert such effects in the brain, then people that take these drugs may put on weight. Such observations do, in fact, commonly occur in clinical practice. Drugs used to treat psychosis, all, to a greater or lesser extent, block the action of dopamine, and all are known to cause weight gain, with some drugs having more potent side effects than others [17]. Even in people with psychosis, many are overweight before they start treatment, compared to the frequency in the general population, increasing speculation that overeating may play a role in the development of psychotic disorders [18]. We will explore the implications of food addiction later in the book. For the meantime, we simply draw attention to such theories, showing how both the biology and clinical manifestations of these disorders show similar features.

SUMMARY

In this chapter we have reviewed the nature and context of addiction, noting that it shares some features similar to hunger. In fact, one could observe that drug dependence could be described as a ‘hunger’ for drugs. Other common features of drug addiction include difficulty stopping the behaviour, due to the presence of a withdrawal syndrome that manifests when an individual stops. The addict who attempts abstinence knows, either consciously or subconsciously, that taking the substance they have become fond of can relieve these symptoms rapidly. If they do continue to abstain, most of the unpleasant discomfort begins to tail off after about three months. The biology of addiction is also beginning to be understood, such that the chemical dopamine, present in the part of the brain responsible for motivation, is stimulated by addictive drugs, and this chemical plays an important part in severe mental disorders, characterised

29


by psychosis. With this information in mind, we move on to consider whether eating behaviour and various foods show similar characteristics to drugs of addiction? Could this information help us find the key to unlock the modern obesity epidemic?

REFERENCES

[1] Russell MA. Cigarette dependence. I. Nature and classification. BMJ. 1971 5;2(5757):330-331.

[2] Center for Health Promotion and Education. Office on Smoking and Health, United States. Public Health Service. Office of the Surgeon General. The Health Consequences of Smoking: Nicotine Addiction: A Report of the Surgeon General [Internet]. 1988 [cited 2011 Mar 24];Available from: http://profiles.nlm.nih.gov/NN/B/B/Z/D/

[3] Balfour DJK. The neurobiology of tobacco dependence: A preclinical perspective on the role of the dopamine projections to the nucleus. Nicotine and Tobacco Research. 2004;6(6): 899-912.

[4] Blumberg H., Cohen D, et al. British Opiate Users: I. People Approaching London Drug Treatment Centres. Substance Use and Misuse. 1974;9(1): 1-23.

[5] APA. Diagnostic and Statistical Manual of Mental Disorders. Washington DC: American Psychiatric Association; 1995.

[6] WHO| International Classification of Diseases (ICD) [Internet]. [cited 2011 Mar 24];Available from: http://www.who.int/classifications/icd/en/

[7] Ainslie G. Breakdown of Will. 1st ed. Cambridge University Press; 2001.

[8] Heather N. A conceptual framework for explaining drug addiction. Journal of Psychopharmacology. 1998;12(1):3-7.

[9] West R, Schiffman S. Smoking Cessation. Fast Facts: Indespensible Guides to Clinical Practice. Oxford: Oxford Health Press Limited; 2004.

[10] Kozlowski LT, Wilkinson DA, Skinner W, Kent C, Franklin T, Pope M. Comparing Tobacco Cigarette Dependence With Other Drug

30

http://profiles.nlm.nih.gov/NN/B/B/Z/D/


Dependencies. JAMA: The Journal of the American Medical Association. 1989 Feb 10;261(6):898 -901.

[11] Tzschentke TM. The medial prefrontal cortex as a part of the brain reward system. Amino Acids. 2000;19(1):211-9.

[12] Drevets WC, Gautier C, Price JC, Kupfer DJ, Kinahan PE, Grace AA, et al. Amphetamine-induced dopamine release in human ventral striatum correlates with euphoria. Biological Psychiatry. 2001;49:81-96.

[13] West R. Theory of addiction. Oxford: Blackwell Publishing; 2006. p. 10.

[14] Munafo M, Albery I. Cognition and Addiction. Oxford: Oxford University Press; 2006.

[15] Laruelle M, Abi-Dargham A. Dopamine as the wind of the psychotic fire: new evidence from brain imaging studies. J Psychopharmacol. 1999;13(4):358-371.

[16] Batel P. Addiction and schizophrenia. European Psychiatry. 2000;15(2):115-122.

[17] Baptista T. Body weight gain induced by antipsychotic drugs: mechanisms and management. Acta Psychiatrica Scandinavica. 1999;100(1):3-16.

[18] Peet M. Diet, diabetes and schizophrenia: review and hypothesis. The British Journal of Psychiatry. 2004;184(47):s102-105.

31

Chapter 3

CARBOHYDRATES, SUGARS AND HUMAN HEALTH: A SUMMARY OF THE EVIDENCE

INTRODUCTION

In the first chapter, we explored recent trends in food intake during the 20th century, preceding the modern day obesity epidemic, starting from the 1970s to present. Two different national or cultural dietary changes preceded the English speaking, collective popping of buttons in the early 1980s to the present day. Anglophones, driven by a desire to reduce the burden of cardiovascular disease, initially in the United States, strove to reduce the fat intake of the populace. Although the macronutrient target changed from all fat, to animal derived, saturated fat; the message was often confused, with “99% fat free” a common health claim, adorning labels everywhere on manufactured food products. Once, when shopping with my son, I (ST) was shocked to see that marshmallows were proclaiming their nutritious properties, with large type “99% fat free” smeared over their plastic wrapper!

Contrary to this anti-fat trend, Asian countries have followed an opposite trajectory, increasing the proportion of fat in their diets, as their economies have strengthened and more expensive animal fat has been more widely affordable. Similarly, obesity statistics in these countries

couldn’t be more different: in the OECD, English speaking countries have lead the stakes, with obesity barely raising a murmur in either Japan or South Korea. In this chapter, we consider, more carefully at an individual and clinical level, what effect modifying carbohydrate intake has on health, and contrast these effects with other diets. From chapter 2, we have reviewed the subject of addiction, concluding that the concept of withdrawal shares some similarities with hunger, usually applied to food. From our medical training we were once firm believers in the supposed adverse health effects of eating calorie rich fat, but what about carbohydrates that have filled the void created by fat in the last thirty years? Are carbohydrates potentially harmful or healthy when consumed in large amounts? Do they contribute to weight gain, and are there any potential properties of carbohydrates that can help us understand the modern epidemic of obesity?

In our medical training, we received little information about the effects of carbohydrates on health. With the benefit of hindsight, we now attribute this to the dominant theory of the time, which emphasised energy density as the most important aspect of food by which one could adjudicate food as good, bad or otherwise. Because fat has twice the energy density of other macronutrients, protein or carbohydrate, the finger of nutritional blame was always pointed at greasy targets. Basic biochemical pathways were, however, taught. I soon realized that the brain, perhaps the most critical organ, on which human survival depends, runs almost entirely on an uninterrupted supply of the single sugar, glucose. The body possesses a neat mechanism by which alternative fuels can be mobilised in the event of a prolonged carbohydrate drought; however, this was presented as a quirk of nature rather than being of much relevance to health or weight loss. Carbohydrates were also relevant to the metabolism of individuals who suffered from another disorder, diabetes. People with this condition have poor regulation of glucose, through either immune destruction or exhaustion from overwork of the visceral organ, the pancreas, which secretes insulin, the primary regulator of glucose levels in the body. Interestingly, the alternative brain fuel, ketones, produced in the starving

Carbohydrates, Sugars and Human Health

state, are also switched on in one form of diabetes (type I), characterised by a complete lack of insulin.

First, what are carbohydrates? Most people are familiar with the concept now with the popular diets that we will explore. Some misconceptions and confusing terminology abound, however. The most common types of carbohydrate are starches, which form the backbone of most diets around the globe. Starch consists of long chains of glucose molecules, linked to form long chains. Starchy products include anything made up of white flour, such as bread, baked goods, pasta, semolina; root vegetables such as potatoes and taro, and other staples such as rice and maize. Glucose exists as a simple sugar, with a sweeter taste and is often added to sports drinks to provide instant energy. Glucose is familiar territory for most doctors. After glucose enters the body, the gut organ, the pancreas, secretes insulin into the blood, so that the body can take up the glucose into the liver and muscle. The body possesses complex machinery for keeping the levels of glucose reasonably stable in the body, so that the precious grey matter within the brain is constantly supplied with enough fuel to keep us going. If the level of glucose drops below a certain threshold, people with low blood glucose levels experience ravenous hunger, become sweaty and faint, and eventually drop unconscious. People with diabetes are not able to regulate the levels of this sugar in the blood, usually due to either a lack of insulin, or insensitivity to this hormone and high levels of glucose can be measured in the veins of people diagnosed with the disorder, before they are treated. Treatment of diabetes, at present, is based on reducing the levels of glucose in the blood by increasing the levels of insulin either by taking drugs that stimulate insulin release or by injecting the substance directly under the skin. Manipulation of the diet of people with diabetes is another way of improving blood sugar, although this has been more controversial. Monitoring blood glucose levels, hence, becomes the obsession of people with diabetes, and the doctors charged with their care.

With the treatment of diabetes centered squarely on glucose, another monosaccharide found in table sugar has received much less attention in the research world until relatively recently. I (ST) confirmed this fact,

35


when I began to read about the health effects of fructose, I wondered why I hadn’t heard anything about this sugar during my training. I scouted in the university library for a text book of clinical nutrition, flicked to the index and looked under ‘f’ for fructose. Nothing. I couldn’t believe it, so I picked up another, then another. The same result. Until the last five years or so, fructose has been off the nutrition radar for all but a small handful of researchers. Sugar is slightly different to glucose. It consists of two sugars joined together to form a disaccharide: one is the familiar building block of starch, glucose, while the second is the enigmatic monosaccharide, fructose. As the name suggests, fructose is found mainly in fruit. Fructose is most concentrated in table sugar, and to a lesser extent, in honey. In sugar, fructose makes up about 50% of the weight of the crystalline substance, joined to glucose as the disaccharide, sucrose. High fructose corn syrup, as the name suggests, is a synthetic derivative of the starch derived from corn. When corn starch is boiled down to break the chemical bonds, free glucose is left. To make something like sugar, an enzyme is added, which converts some of the free glucose to fructose. High fructose corn syrup is the sweetener most commonly added to manufactured foods in the United States and Canada. Due to governmental subsidies for corn growers, high fructose corn syrup has become the most economically favorable sweetener for the North American food industry. The only difference between this product and sugar is that the glucose and fructose exist in free, single sugar, monosaccharide form in high fructose corn syrup, whereas table sugar consists of the two single sugars joined by a chemical bond as the double sugar sucrose (figure 1). With glucose being easy to measure in patient’s blood, and defining the diagnosis of diabetes, it is easy to understand why fructose has been largely ignored as a focus of nutrition research. What is more, fructose is found in fruit, what could possibly wrong with eating fruit? We return to fructose later in the chapter, as a relatively late development in the carbohydrate story. We first consider whether diets based on modifying carbohydrates, either in total, or based on glucose have shown any benefits to human health.

36


Figure 1. The constituents of table sugar, glucose and fructose, free as present in high fructose corn syrup, and joined at the hip, as sucrose, found in table sugar.

PHYSIOLOGY OF GLUCOSE AND INSULIN The first clue that I had that carbohydrates may be important in the

regulation of weight was observed in people with type 1 diabetes, more common in children, who produce little or no insulin. The lack of this pancreatic hormone occurs because their own antibodies have, for an unknown reason, destroyed their cells that produce the protein. Diabetes specialists know that young women with this disorder, who are often obsessed with their weight, will reduce their insulin dose, from prescribed levels, to shed a few pounds. Although these patients may be admonished by their doctors about the long term adverse consequences of such

37


behaviour, living with precariously high levels of glucose coarsing through their veins - causing rotten eyes, limbs and heart muscle - the immediate desire to control weight may be too strong. The first lecture that I received on the subject of this type of diabetes at medical school acknowledged this seeming paradox, that diabetes was “starvation in the face of plenty”. Before effective treatment to reduce blood glucose was available, sufferers of diabetes could seemingly eat to excess and lose weight simultaneously, all because of the lack of a crucial hormone that was critical for processing glucose into stored energy or body fat.

Despite the apparent centrality of insulin to weight regulation in patients, beliefs handed down from academics for the apparent excess weight and skyrocketing rates of diabetes was generally attributed to energy density. People with diabetes acquired the disease from fat and not sugar. From the observation that fat contains twice the energy per unit weight (energy density) than either of the two other macronutrients, protein or carbohydrate, this rather simplistic, but seemingly elegant principle, enshrined the basis of public health and nutritional strategies to treat the growing tide of people with diabetes that were beginning to swamp health services.

HEALTH EFFECTS OF CARBOHYDRATE MODIFIED DIETS

Which diets are commonly used that are based principally on modifying carbohydrates?

The Atkins’ diet [1] consists of almost abandoning carbohydrate altogether, no more than 20g per day or less than one slice of bread is allowed in the early phases. On the other hand, Atkins lets dieters eat as much fat and protein as their heart desires, a polar opposite to usual nutritional approaches of limiting fat and total energy.

Although the Atkins diet has been lampooned in nutrition circles for almost half a century as antithetical to interventions grounded on energy density, another carbohydrate based-diet, which measures the intensity of the blood glucose response from a standardised portion of food has become

38


more accepted into the mainstream of nutritional thought. First developed in the 1980s, glycemic index (GI) is a measure of what effect a food, altered in size to include 50g of carbohydrate, has on the area under the curve of a blood glucose (an indicator of the average glucose level) vs time graph [3]. Pure glucose is the reference standard, designated 100, by which all other foods are compared. Starchy foods are highest, for example, white bread is about 70, with whole grains, such as lentils, and fruit and vegetables generally lower - in the 30s and 40s.

The so called “low glycemic index” diet consists of eliminating consumption of foods whose glycemic index is greater than an arbitrary figure of about 55. The diet was initially considered most useful in lowering blood glucose in people with diabetes, which is thought to reduce the onset of complications from the disease [4]. In such people, blood glucose becomes elevated, and higher average levels correlate with increased adverse effects. Indeed, much of the treatment of diabetes is focused on reducing blood glucose through the use of both medicines and insulin, and limiting the intake of starchy foods. As long chains of glucose, starch is broken down and, following absorption, results in a spike of glucose in the bloodstream. If glucose levels could be controlled through diet, lowering dependence on drugs, then surely this strategy might improve the health of people with diabetes. Given that this condition is a relatively arbitrary cut-off at one end of an extreme end of the spectrum of glucose control, maybe everyone would be better off eating low GI food? Also, insulin is an important hormone which promotes the laying down of fat, encouraging the liver to convert a digested glucose meal to cholesterol which is then transported in the blood stream to the periphery and stored as excess flab. Insulin release follows a glucose meal, so that choosing foods that do not produce such a large bolus of glucose would theoretically improve average glucose levels, help people lose weight and reduce the chance of them developing life threatening complications of diabetes such as heart attacks or strokes. Because less insulin is produced, then theoretically, such a diet would also help people lose weight.

So much for the theory, what has been born out in reality? Although very skeptical about the adverse effects of carbohydrates, the medical

39


literature continues to fill with evidence that diets based on eating low glycemic index foods result in greater weight loss and better health outcomes than traditional diet methods (reducing energy density or fat). Such is the volume of studies on glycemic index that some researchers have pooled many studies to look at the overall effect of the diet on weight loss and risk of developing chronic disease, using a technique called meta-analysis. Such studies are often accorded the highest level of evidence, among the hierarchy of scientific evidence. Two influential so called “meta-analyses” have been published, one demonstrating that people following glycemic index diets reduce their weight [5] with another showing reduced risk of a range of important and common chronic diseases from such a diet [6]. One study, which used a similar technique to compare a range of dietary techniques at reducing risk of heart attack showed that glycemic index was in the top four methods to lower one’s chances of such an outcome [7]. According to the study, the best means of reducing risk of a heart attack was the Mediterranean diet, which again, emphasises the intake of unrefined, low-glycemic-index, carbohydrate food.

In patients with diabetes, an American endocinologist, Eric Westman, compared a low glycemic index diet with the Atkins diet to assess their effects on glycemic control, weight loss, blood pressure and other indices of cardiovascular risk [8]. The results were astonishing. Although many subjects dropped out of the study (41%), the Atkins diet group had most weight loss at 6 months (-11 vs -7kg) and almost all no longer needed drug treatment for diabetes (95% compared to 62%). Such results strongly indicate that both diets help reverse the metabolic effects of type 2 diabetes, but reducing all carbohydrate seems to confer additional benefit, over only limiting high glycemic index, or starchy foods. Later we speculate that glycemic index overlooks the effects of an important sugar – fructose. Perhaps the main difference between the two groups, in this trial, was fructose intake?

With such glowing evidence, has use of the glycemic index or Atkins (low carbohydrate diet) become common place in medical practice to help people control their weight? The answer is that it has and it hasn't.

40


Nutrition ideas are slow to change, and as we have discussed in chapter 1, the public health and medical community, lead by the American Heart Association, has campaigned against the intake of fat and saturated fat to lower heart disease risk. One of the side effects of this advice, although often not acknowledged, was to increase the amount of carbohydrate consumed. Also, public health professionals are fond of simple messages to convey to the public. The message to reduce fat is easy. Most people recognise fat on meat and know the greasy feel of fried food. Such a message is easily communicated and understood. Glycemic index, in contrast, is complicated, and takes more effort to convey to the public. Also, when the low fat message is combined with the low glycemic index one, they may appear contradictory and confusing. If you are admonished to reduce fat, your only recourse is to eat either protein or carbohydrate. Protein supply is often limited due to expense (animals are costly to cultivate), so carbohydrate naturally floods the void created by the low fat diet. What is not often stated is the contradictions between the low fat and low (or modified) carbohydrate approaches. Fat, taken with carbohydrate, actually delays the emptying of the stomach and so, in a purely mechanical fashion, lowers the GI of a carbohydrate meal. Protein and acid have a similar effect, slowing down the rate at which the stomach, the body’s food storage bag, empties, allowing the nutrients to be absorbed by the small intestine. Glycemic index and low fat diets are uncomfortable bed fellows.

Has the glycemic index diet been popular? In contrast to the reticence shown by the medical profession, the glycemic index range of books, published by an Australian group from the University of Sydney, have certainly been successful in marketing their ideas. The continually iterating versions of the “New Glucose Revolution” consistently hits the best seller lists on Amazon, and the penetration of glycemic index into the Australian psyche has been dramatic. The “GI” symbol, signifying a low glycemic index food is commonly found on products displayed on Australian supermarket shelves. No more than 1,000 kilometres away in New Zealand, a country that shares similar cultural traditions with Australia, has little recognition of glycemic index, and the “GI” symbol is not widely displayed. For example, a new refined, low-GI table sugar, recently

41


marketed in Australia, rapidly claimed 4% of the supermarket sugar market, however, the same product, on sale in New Zealand, struggles to reach supermarket shelves.

Initially, we were taken with glycemic index. When seeking to identify a property of food that may predict its addictive potential as well as having proven effects on human health, glycemic index appeared to fit the bill. What we found puzzling was that, in general, glycemic index ranks some refined carbohydrate laden foods higher (more dramatic glucose response) and whole foods lower. Sugar, however, is an important exception. We know from global records of food production, import and export that sugar intake has risen substantially, and is one of the most dominant nutrition changes in the latter half of the twentieth century [9]. The country with the most dramatic sweetening of their food supply, the United States, also has the highest proportion of obese adults of all industrialized nations. However, if you believe the glycemic index is the most important predictor of the health value of food, sugar appears relatively benign. Pure sucrose has a GI of 68 [3], and many sugar containing products have lower GIs, due to either their fat content. The most popular book written on the effects of the glycemic index actually encourages its readers to enjoy eating sugar [3]. What is it about sugar that gives it such a low GI, despite it being a highly refined substance? Does sugar have any special properties which may cause weight gain or other diseases to occur in people with a sweet tooth?

SUGAR

Fructose holds the key to understanding the effect sugar has on health. Sugar, the variety you buy in the supermarket, is derived from sugar cane, with only one substance left after all the other parts of the plant are stripped away in the refining process: sucrose, a molecule consisting of one part glucose and one part fructose, chemically linked. Molasses, a black, tarry, licorice tasting goo is made early in the process of making sugar from sugar cane. In the United States, as we mentioned earlier, sugar

42


contained in manufactured foods is slightly different, usually derived from corn (high fructose corn syrup).

What is unique about sugar (or HFCS) is its concentration of fructose-roughly 1:1, or 50% by weight, which is much higher than naturally occurring sources. Fructose is also found in fruit, honey and some vegetables, however, the sugar in these items is far less concentrated (bananas contain about 10% fructose). Fructose has often been ignored in nutritional circles, because, it is assumed that since it is found in fruit, which have been a key part of low fat diets, so it must be harmless... or is it? Can something that nature provides be bad for us?

Studies of human risk perception show that naturally occurring hazards are thought to be much less dangerous than those that are man made [10]. For example, radioactive waste is likely to engender more fear than say tobacco, even though the latter causes far more deaths. Also, risky exposures we come across every day are perceived as much less important as rarely encountered ones. Sugar is often considered a “natural” sweetener, particularly when contrasted to low calorie counterparts such as aspartame and sucralose. However, the briefest glance into the manufacturing process, by which sugar cane is turned into table sugar, indicates that this process is far from “natural”. Sugar cane is crushed, mixed with lime, and then mixed with a number of chemicals, such as phosphoric acid and calcium hydroxide, to produce white sugar. Sucrose, in high (99%) concentration is left, with all other plant material stripped away.

If we leave the argument over whether sugar is “natural” to one side for a moment, we now consider whether sugar affects health, and if so, how? Interestingly, in the late 1990s and early new millenium, the American Diabetes Association advocated increasing fructose consumption in people with diabetes [11]. It seems counter-intuitive to most people without nutritional training to advise people with diabetes to eat sugar, but that was a policy, and I even came across a jar of jam recently that claimed to be healthy due to its high fructose content. This policy was derived mainly as a result of fructose's modest short term effect on the glucose level in the blood, after a sugary or fruity meal. Much of the damage from

43


diabetes is thought to accrue from high levels of glucose circulating in the blood vessels of patients with diabetes, and if fructose intake may improve such a measure, then surely it must be safe, right?

Figure 2. The different metabolic paths of glucose and fructose.

The theory behind this advice was that fructose did not increase blood glucose levels, because it is broken down by the liver, after being absorbed in the gut, and before it enters the blood stream, where it can be easily measured. Because treatment for diabetes is based on measurement of, and control of blood glucose, diabetes experts initially considered fructose harmless. Fructose, unlike glucose, does not stimulate insulin release and because it is commonly found in fruit, it was thought to be a healthy alternative for people whose bodies suffered from a lack of insulin, or sensitivity to the hormone, and couldn't process glucose properly. Fructose is taken up by the liver independent of insulin (Figure 2), and could spare the body from potentially harmful exposure to glucose. However, it was soon found that fructose had adverse effects on fat levels in the blood,

44


being readily converted to this form of energy storage, in contrast to glucose that is mostly used for energy. High fructose intakes unequivocally raise serum triglycerides levels [2]. Although debate continues about which subgroup of fats found in the blood cause heart attacks (high density lipoprotein is probably the strongest contender), high triglyceride levels have been linked to heart attacks in several observational studies [12]. Although these downsides of fructose have been largely conceeded, and advocates for fructose have withdrawn advice to consume sugar as a health food, a rising tide of evidence indicates that fructose not only contributes to high triglyceride levels, but also give rise to a range of other common and devastating diseases.

Animal studies have documented adverse metabolic effects of refined fructose intake. Rodents fed on high fructose and sucrose diets, but not high glucose diets, develop features of the metabolic syndrome, such as hyperinsulinemia, hyperuricemia and hypertriglyceridemia [13].

To explore the effect fructose may be having on our health, we consider in more detail the physiological effects of fructose, before reviewing possible health effects of excess consumption. A full discussion of the metabolism of fructose is beyond the scope of this chapter, but is discussed elsewhere [13]. After eating, fructose is absorbed from the small bowel and enthusiastically broken down by the liver, independent of insulin. Unlike glucose, fructose does not stimulate insulin release, which signals fullness or satiety. Metabolism of fructose depletes cellular energy stores (ATP), and induces uric acid production (which causes a particular type of arthritis - gout). The principal products of liver fructose break-down are triglycerides, which are then released into the blood. While fructose is processed, conversion of glucose to glycogen (glycogenesis) in the liver is blocked. The reduction in glucose processing by the liver, in turn, causes insulin levels to rise so that glucose is taken up in alternative sites, such as muscle tissue. As a result of high insulin levels, muscles compensate by becoming insulin resistant. Such a mechanism may explain how fructose has little acute effect on serum glucose levels, but importantly, impairs blood glucose control after long term exposure to high doses.

45


In contrast to animal studies, links between fructose intake and disease outcomes have not been so conclusively demonstrated in humans, although regimens with longer follow up periods and higher doses of fructose (>200g/day or the equivalent of two cups of sugar/day) tend to produce clearer links with risk factors for disease. For example, small intervention studies have shown that high doses of fructose provoke insulin resistance within one week [14], whereas smaller doses (<100g/day or the equivalent of one cup per day) do not provoke insulin resistance and may conversely improve the ability of the body to regulate blood glucose [13]. Fructose consumption acutely raises blood pressure after short term exposure in normal young men compared to water and glucose controls (mean change in systolic blood pressure from baseline 4mmHg, 2 hours after 60g meal, compared to a 1 mmHg change in both control groups) in a cross-over design [15]. A rise in systolic blood pressure of 7 mmHg was observed after two weeks treatment with 200g of fructose per day in a randomised trial (74 individuals took part in the study) [15]. This trial also found adverse effects on triglycerides, fasting insulin and the number of people that met the criteria for metabolic syndrome (a cluster of metabolic indicators which indicate high risk of cardiovascular disease). Other effects of fructose consumption include modest weight gain in some short term intervention studies [16]. The health effects of long term, high dose exposure of fructose have not been rigorously studied in randomised controlled trials. Given the consistent evidence of adverse effects of high dose fructose in short term studies, giving the carbohydrate long term at such a level is likely to be hampered by ethical stumbling blocks to conducting such a study.

Perhaps the most investigated effect of fructose intake, in humans, is the deterioration in blood fat profiles. A meta-analysis indicated a consistent effect of fructose worsening serum triglyceride concentrations in experimental studies of patients with diabetes, compared with control diets [2]. Increasing evidence supports the association between triglycerides and coronary heart disease, although abnormal triglyceride rich lipoproteins are commonly associated with other adverse lipid abnormalities (raised low density and diminished high density lipoprotein cholesterol concentrations)

46


which complicate debate about which lipid fraction is causally associated with coronary outcomes [17].

Although the evidence continues to grow that fructose damages health in short-term randomised studies, the evidence for long-term, high-dose, consumption has not been similarly investigated. Probably the best evidence that such exposure causes harm comes from studies of the link between soft drink intake and poor health. Given that sugar-sweetened soft drinks represent a large share of the added sugar in the modern diet, drinking such beverages may be considered a rough indicator of sugar exposure in the diet. Systematic reviews of observational studies of the effect of sugar sweetened soft drinks on disease outcomes consistently show positive associations. For example, a meta-analysis of longitudinal studies investigating the correlation between sugar sweetened drinks and increased body weight, showed an r-value (a measure of correlation) of 0.09 (P =0.001; a statistic indicating that the finding is unlikely to be due to chance) [18]. Studies were less likely to show a positive association if they included weaker-designs, such as cross-sectional studies or were industry (sugar and soft drink) funded. As well as sugary drinks contributing to these outcomes, the opposite, limiting fructose consumption, improves individual's health. For example, an experimental randomised study (considered stronger evidence than observational studies) in which obese adolescents were given either supplemental soft drinks with artificial sweeteners (to replace sugared varieties) or no intervention found a beneficial effect on body mass index, with effect modification, such that largest effects were observed in people who were most overweight at the start of the study [19]. Although clinical trial evidence is scanty, the results of a small number of randomised studies indicate that high fructose diets contribute to the disease cluster which includes risk factors for heart attacks and diabetes, known as metabolic syndrome. This includes a cluster of characteristics such as obesity, high blood pressure, pre-diabetes caused by lack of sensitivity to insulin, and an adverse blood fat profile with high triglycerides and low high density lipoproteins.

47


Stepping outside the familiar (at least to us) world of medicine, perhaps the best evidence for poor health, as a result of excess sugar in the diet, stems from the observation that sugar eaters develop rotten teeth. Although, surprisingly, the link between sugar consumption and dental caries is still controversial, the British Nutrition Foundation sum the evidence best when they stated

“the evidence establishing sugars as an aetiological factor in dental caries is overwhelming. The foundation of this lies in the multiplicity of studies rather than the power of any one.” [20]

The authors go on to state that starch and other macronutrients are unlikely to contribute to oral decay. If this is so, then the presence of dental caries indicates, with some precision, lifetime exposure to sugar. Presumably, the severity of caries may be modified by brushing or flossing and visiting one's dentist, however, these factors are likely to be small compared to dietary sugar intake. If, as we allege, sugar causes elements of metabolic syndrome, which, in turn, raise the risk of heart disease, then we might expect dental caries and heart disease to be closely linked. Or at least, people with rotten teeth have a higher risk of developing heart attacks than those with a full set of pearly whites. So, several studies have demonstrated high rates of decayed, missing or filled teeth in a cohort of individuals who required hospital treatment as a result of either a heart attack or angina [21]. Such a link persists, even after adjusting for risks for such conditions, such as high blood pressure, diabetes, blood cholesterol, age and gender. Adding to this evidence, a recent analysis highlighted the close link between added sugar intake and levels of blood cholesterol levels (raised levels of ‘bad’ cholesterol – LDL; low levels of good cholesterol – HDL and high levels of triglycerides), from the largest health survey undertaken in the United States, the NHANES [22]. Such evidence points to sugar not only causing weight gain, but that it is also directly implicated in the epidemic of coronary artery disease that has been the leading cause of death in developed countries since the latter half of the twentieth century.

48


Interestingly, the link between rotten teeth and heart attacks has been attributed to the role of the proliferation of bacteria in the mouth, and the inflammation that commonly occurs in the teeth and gums. A simpler explanation, derived from our observations that high levels of fructose in the diet leads to risk factors for heart attacks, such as low levels of good cholesterol, high blood pressure and weight gain, is that bad teeth are an indicator of sugar intake, and it is this exposure, primarily, that drives the link between dental decay and heart disease (figure 1).

Figure 1. A plausible causal diagram explaining the nature of the association between dental decay and coronary heart disease. Solid arrows indicate proposed direction of causation while dashed arrow shows apparent association.

Along with developments in such areas, a slow revolution has been underway in the understanding of how diseases such as gout and irritable bowel syndrome are caused. Gout is a very painful arthritis that is most common in middle-aged and older men. The disease results from excess build up of uric acid in the body, which, at a certain point starts to precipitate out as needle like crystals in the small joints of the hand and foot, although larger joints may also be affected. People who suffer from gout often have other risk factors for heart disease, such as high blood

49


pressure, diabetes, obesity and a poor lipid profile. The treatment consists of acute pain relief, along with drugs which reduce the rate of build-up of urate in the body.

The history of the disease is interesting. It was first described among the royal elite in European countries, before establishing a presence among the hoi polloi. The dietary habits of the royals during the 16 th, 17th and 18th

century was notable for a fondness for sugar. Indeed, one of the first converts to the sweet substance was Queen Elizabeth, who was often painted with her mouth closed, due to the devastating effect her love for sucrose wrought on her dental work [23]. When training at medical school, the official nature of the cause of gout was under investigation. Gouty attacks, which are often memorable and exquisitely painful, were, we were told, often provoked by meals heavy in the building blocks of life – purines and pyrimidines from an animal’s genetic material (DNA). Such meals included shell fish, alcohol, and meat. However, in the recent past, increasing evidence from observational studies suggests that sugar (fructose) plays a role. Laboratory scientists have established that uric acid is an important byproduct of the breakdown of fructose. If this is true, then we might expect to see that people with gout have higher intakes of sugar. This has recently been confirmed in a study by Choi [23]. The study showed that the excess risk of drinking between one and two soft drinks per day doubled the chance of women developing gout throughout the study. Curiously enough, despite such evidence coming to light, the impetus to restrict sugar intake among people with gout has been very slow to emerge.

In line with the growing evidence that we have conveyed here, that sugar is associated with a host of indicators of risk for premature cardiovascular disease, the American Heart Association has published two remarkable papers, only seven years apart, which took almost polar opposite stances on the issue of sugar in the diet. In 2002, the Association reported that

“...Consuming fructose either free or in the form of sucrose has neither beneficial or adverse effects... .” [25]

50


They went on to advise doctors that the case against sugar was not conclusive and that individual doctors should advise their patients according to their own professional judgment.

Seven years later, the advice had changed. The tide of evidence against sugar had accumulated to the point that links with obesity and diabetes were stated, and the about face in policy direction was acknowledged.

“Originally proposed as the ideal sweetener for people with diabetes... Fructose... has been indirectly implicated in the epidemics of obesity and type 2 diabetes”. [26]

Perhaps the most surprising advice was the latter paper’s conclusion. In the past, nutritional advice to restrict free sugar has been couched in terms of the proportion of daily energy intake. In New Zealand, the Ministry of Health Food and Nutrition Guidelines admonish adults to restrict sugar intake to less than 15% of total daily calories, due to the excess energy provided from this source and the risk of developing dental caries. This is not only very opaque, almost no individual knows their own daily energy intake, but also fairly lax. If one would like to eat more sugar, according to such guidelines, one only needs to increase one’s daily intake of energy. How do we, as a nation, measure up to this level of consumption? Long term trends of individual food and nutrient consumption in New Zealand are difficult to assess, however, population aggregates exist. One such source is United Nations Food and Agriculture Organisation (UNFAO) food balance sheets [26]. To re-iterate, the balance left from food produced, minus export, plus import is considered to have been consumed, which is then divided by the total number of the population to yield a per capita value. From this data, we observed a worldwide trend toward higher levels of sugar consumption, with a roughly 30% increase over the last thirty years. In addition, the average level of sugar intake in English speaking countries is very high, at about 40 teaspoons per day per capita. In New Zealand, for example, we are on track with sugar limits of 15% of daily energy. In 2007, the energy derived from raw sugar from UNFAO data was almost exactly 15% of the total consumed. The total number of teaspoons consumed, however, is rather high on a global scale, at about 36 per day. In the United States, the

51


average daily sugar intake is about 40 teaspoons per day. Against this backdrop, the revised advice from the American Heart Association was to restrict the sugar intake to no more than six teaspoons per day for women, and nine for men. Assuming people in the US all consume 40 teaspoons per day; this is an average decrease of about one sixth. The paper did not elaborate the population implications of such advice. To effect such a change, as the paper suggested, through individual clinical interactions, seems to me, almost as effective as King Canute ordering the tide to stop coming in. Clearly, if these guidelines were taken seriously, they have far reaching implications for the nature of the food supply to almost all English speaking countries (and many others), whose diets are heavily fortified with sugar.

In this chapter, we have written about the role of carbohydrates and fructose in causing risk factors for major causes of death in Western countries. However, there are other areas in which fructose may play a role. For example, fructose exposure during pregnancy is an emerging area, with scientists that work with rodents beginning to investigate the effects on the developing foetus. In an ecological study, in which data is grouped at the country level, we found a link between levels of childhood asthma, and per capita sweetener consumption, measured from food disappearance data immediately before birth (Figure 3) [28]. Surprisingly, little is now known about what causes asthma to develop in childhood, with many theories not showing promise under close scrutiny. For example, many exposures which exacerbate asthma once an individual has the disease, such as air pollution, owning pets, or having the cold or flu, have not been able to explain the variation between countries. Our study explained some of the high levels of asthma reported in English speaking and Latin American countries, with the common factor high levels of sugar intake. Although we cannot be certain that sugar is the cause of asthma, the study is a promising lead, and fits in with other observations which document the concurrent rise of obesity and asthma in the latter part of the twentieth century. This is one area in which sugar consumption is showing promise as a potential cause for a variety of diseases that are becoming more prevalent in the latter part of twentieth century. We speculate that if

52


sugar is causally associated with obesity, many of the diseases associated with obesity, such as cardiovascular disease (as we have already discussed) and many types of cancer, may have sugar (fructose) consumption as a root cause. Time will tell, and further studies are awaited which explore the relationship between sugar and other disease outcomes.

WHAT ABOUT FAT?

This chapter has discussed, at some length, the potential adverse effects of sugar and carbohydrates. How does this compare with other nutrient exposures that may be harmful to health? We do not have the time to have a full discussion about other macronutrients, however, it is useful to discuss the impact of fat consumption and saturated fat intake, because, as we discussed, these were the driving forces behind early public health nutrition behavior change messages. Recently, an uncomfortable feeling has surfaced among public health nutritionists, that saturated fat may not have any effect on coronary artery disease, contrary to the dogma that surfaced in the 1960s and 1970s. Several meta-analyses, combining the results of individual studies, have shown no statistical link between eating saturated (predominantly animal) fat and developing coronary heart disease, or the more general category, cardiovascular disease, which includes stroke and blocked blood vessels in legs and arms [29]. These studies are assumed to be the highest level of evidence, short of randomized studies, which are infrequently conducted to evaluate the effect of food on disease outcomes. Some researchers have stuck to their guns, claiming that these studies do not matter, and the wealth of other data supporting the saturated fat hypothesis over rules such studies.

Have any studies compared low fat to low carbohydrate diets directly? Perhaps the best evidence we have seen to date that compares the two approaches, was recently published in the Annals of Internal Medicine [30]. The trial randomized a cohort of obese adults (307 subjects) into either a low fat or low carbohydrate intervention. Both groups maintained significant weight loss at two years follow up (mean weight loss 7kg at two

53


years), however, the low carbohydrate group had superior indices of cardiovascular risk than the low fat group. Both blood pressure and serum lipid profile favoured the low carbohydrate group.

We find it alarming that the historic imprinting of the low fat message, predating the modern obesity epidemic, may have been hot air. It supports our view, that in general, low fat campaigns have pushed the populace toward increased carbohydrate consumption and that such a policy may be, paradoxically, partially responsible for the modern day obesity epidemic.

54


Figure 3. Severe asthma symptom prevalence in 6 and 7 year old children plotted against average per capita added sugar consumption, 7 years prior, by country. Solid line shows log-linear regression line with dashed lines illustrating 95% confidence interval.

SUMMARY

In this chapter, we have established that intake of carbohydrate plays an important role in human health. Although, as discussed in earlier chapters, the principal advice from nutritional and medical authorities since the 1960s to present, has trumpeted the adverse effects of fat on health, primarily obesity and risk of future heart disease. The side effect of this advice, perhaps unintentional, has been to open the door to unrestrained carbohydrate intake. The proliferation of nutrition claims, based on the

55


absence of fat (for example, the ubiquitous “99% fat free” label), glosses over the uncomfortable reality that such foods are usually fortified with carbohydrate and added sugar to replace the lost fat. This, so called, nutritional wisdom is an interesting example of scientific reductionism; whereby the absence of one nutrient, purported to have adverse health effects, trumps the bigger picture of what the food contains. We have argued, that despite a preoccupation with fat, evidence indicates that high levels of refined carbohydrate causes a range of important chronic diseases – particularly heart disease and cancer. From earlier chapters, we observed that the proportion of people considered obese has escalated, particularly in English speaking countries, which has been correlated in time with earlier advice to reduce fat intake. Whilst glycemic index is one established measure of the effects of carbohydrate on the body, it only considers the presence of glucose, while the sweetest of all simple sugars – fructose - is ignored. Researchers now claim that fructose contributes to obesity, high blood pressure, and diabetes, all of which raise the risk of early heart attacks. In the next chapter we consider the spectrum of food, and discuss the evidence that different foods are addictive.

REFERENCES

[1] Atkins R. Dr Atkins New Diet Revolution. London: Vermillion; 2003.

[2] Sievenpiper JL, Carleton AJ, Chatha S, Jiang HY, de Souza RJ, Beyene J, et al. Heterogeneous effects of fructose on blood lipids in individuals with type 2 diabetes: systematic review and meta-analysis of experimental trials in humans. Diabetes Care. 2009;32(10):1930-7.

[3] Brand-Miller J, Foster-Powell K, Colagiuri S. The New Glucose Revolution. Sydney: Hodder; 2000.

56


[4] Opperman AM, Venter CS, Oosthuizen W, Thompson RL, Vorster HH. Meta-Analysis of the Health Effects of Using the Glycaemic Index in Meal-Planning. British Journal of Nutrition. 2004;92(03):367-381.

[5] Thomas D, Elliott EJ, Baur L. Low glycaemic index or low glycaemic load diets for overweight and obesity [Internet]. In: Thomas D, with The Cochrane Collaboration, editors. Cochrane Database of Systematic Reviews. Chichester, UK: John Wiley & Sons, Ltd; 2007 [cited 2011 Feb 9]. Available from: http://onlinelibrary.wiley.com/o/cochrane/clsysrev/articles/CD005105/abstract.html

[6] Barclay AW, Petocz P, McMillan-Price J, Flood VM, Prvan T, Mitchell P, et al. Glycemic index, glycemic load, and chronic disease risk—a metaanalysis of observational studies. Am J Clin Nutr. 2008;87:627-37.

[7] Mente A, de Koning L, et al. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Archives of Internal Medicine. 2009;169(7): 659-669.

[8] Westman E, Yancy W, Mavropoulos J, Marquart M, McDuffie J. The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutrition & Metabolism. 2008;5(1):36.

[9] Popkin BM, Nielsen SJ. The sweetening of the world’s diet. Obesity Research. 2003;11(11):1325-32.

[10] Sandman P. Responding to Community Outrage: Strategies for Effective Risk Communication. 1st ed. American Industrial Hygiene Association; 1993.

[11] Taubes G. The Diet Delusion. New York: Vermilion; 2007. [12] McBride PE. Triglycerides and Risk for Coronary Heart Disease.

JAMA. 2007;298(3):336-338. [13] Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang D-H,

et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney

57


disease, and cardiovascular disease. Am J Clin Nutr. 2007;86(4):899-906.

[14] Havel P. Dietary Fructose: Implications for Dysregulation of Energy Homeostasis and Lipid/Carbohydrate Metabolism. Nutrition Reviews.2005;63(5): 133-157.

[15] Perez-Pozo SE, Schold J, Nakagawa T, Sanchez-Lozada LG, Johnson RJ, Lillo JL. Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response. Int J Obes. 2009.

[16] Raben A, Vasilaras TH, Moller AC, Astrup A. Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects. Am J Clin Nutr. 2002;76(4):721-729.

[17] McBride PE. Triglycerides and Risk for Coronary Heart Disease. JAMA. 2007;298(3):336-338.

[18] Vartanian LR, Schwartz MB, Brownell KD. Effects of Soft Drink Consumption on Nutrition and Health: A Systematic Review and Meta-Analysis. Am J Public Health. 2007;97(4):667-675.

[19] Ebbeling CB, Feldman HA, Osganian SK, Chomitz VR, Ellenbogen SJ, Ludwig DS. Effects of Decreasing Sugar-Sweetened Beverage Consumption on Body Weight in Adolescents: A Randomized, Controlled Pilot Study. Pediatrics. 2006;117(3):673-680.

[20] Sheiham A. Dietary effects on dental diseases. Public Health Nutrition. 2001;4(2b):569-591.

[21] Janket S-J, Qvarnstrom M, Meurman JH, Baird AE, Nuutinen P, Jones JA. Asymptotic Dental Score and Prevalent Coronary Heart Disease. Circulation. 2004;109(9):1095-1100.

[22] Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB. Caloric Sweetener Consumption and Dyslipidemia Among US Adults. JAMA: The Journal of the American Medical Association. 2010 Apr 21;303(15):1490 -1497.

[23] Sugar: A Bittersweet History. Penguin Books Canada, Limited; [24] Choi HK, Willett W, Curhan G. Fructose-Rich Beverages and Risk

of Gout in Women. JAMA: The Journal of the American Medical

58


Association [Internet]. [cited 2011 Feb 22];Available from: http://jama.ama-assn.org/content/early/2010/11/10/jama.2010.1638.abstract

[25] Howard BV, Wylie-Rosett J. Sugar and Cardiovascular Disease: A Statement for Healthcare Professionals From the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2002;106(4):523-527.

[26] Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig RH, et al., Metabolism undefined the Council on EPrevention. Dietary Sugars Intake and Cardiovascular Health: A Scientific Statement From the American Heart Association. Circulation. 2009;120(11):1011-1020.

[27] Food UN, Agricultural Organisations. FAOSTAT. United Nations Food and Agricultural Organisations; 2010.

[28] Thornley S, Stewart A, Marshall R, Jackson R. Per capita sugar consumption is associated with severe childhood asthma: an ecological study of 53 countries. Prim Care Respir J [Internet]. 2010 [cited 2011 Feb 22];Available from: http://www.thepcrj.org/journ/citation_export.php?type=part&article_id=767

[29] Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. The American Journal of Clinical Nutrition [Internet]. 2010 [cited 2011 Feb 22];Available from: http://www.ajcn.org/content/early/2010/01/13/ajcn.2009.27725.abstract

[30] Foster GD, Wyatt HR, Hill JO, Makris AP, Rosenbaum DL, Brill C, et al. Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet. Annals of Internal Medicine. 2010;153(3):147 -157.

59

Chapter 4

CAN FOOD BE ADDICTIVE?

INTRODUCTION

We have briefly surveyed the consequences of overeating, leading to obesity and overweight, and seen that this pattern emerged over the last thirty to forty years, mostly in English speaking countries, with Asian countries virtually exempt from this trend. The origins of the obesity epidemic were preceded by the “diet-heart hypothesis”, initially propagated by the American Heart Association, and later spread to other Anglophone nations. The advice, disseminated at that time, was to reduce saturated fat consumption, often simplified, to one thought more palatable - reduce all fat and the arteries feeding your heart muscle won’t get clogged up. Such advice was heeded, both by the populace, and those that feed the populace - the food industry. Suddenly the term “99% fat free” became a health claim, and products that boasted these properties flew off the shelves. Doctors convinced patients to abandon full cream milk for skim milk - milk minus the fat. In contrast, no barbs were pointed toward carbohydrate. Although carbohydrates were not proven innocent, its guilt was never established. The message not to eat fat left the other two macronutrients to fill the void - protein and carbohydrate. Whilst the cost of protein prohibits its widespread consumption, the same can not be said for carbohydrate. Also, animal protein is often associated with animal fat,

something we were told to avoid. While the principal source of protein is animals, carbohydrates mainly come from plants, which are less demanding of agricultural time and resources, and therefore less costly. Economic forces were, without doubt, a strong incentive that drove carbohydrate to become a more important contender in the Western diet. Some studies, however, derived both from the observation of the behavior of rodents and animals, suggests that the message to avoid fat, and so eat carbohydrate, has stimulated strong biological urges and hunger, resulting in a vicious cycle of increased appetites and overeating and obesity.

In previous chapters, we considered what properties of carbohydrates stand out as most likely to be responsible for the adverse health effects of this food group - refined starches and fructose (often found bound to glucose as sucrose). We also touched on features of the clinical syndrome of addiction. We noted that addiction may be considered ‘a hunger for a drug’. Although language related to food is often used to describe addiction, in reality, modern nutrition has developed, effectively ignoring the biological drives that lead to people putting food in their mouths. In this chapter, we review evidence that food delivers reward to motivation centres in the brain, and possesses some properties similar to drugs of addiction. We also consider what subgroups of food are more likely to be rewarding than others, with the potential to cause binging and obesity.

What would we expect from a food, if it were to provoke overeating? What properties would make it “addictive”? What criteria would help us rank foods, based on their addictive properties? These questions are difficult to answer definitively, however, we may guess from studies of other addictive substances. Why are cigarettes more difficult to give up than nicotine gum, for example? We also consider what may be learned from the experiences of obese people when they try and diet. What are their problem foods? What about the reward centre in the mid-brain? Which foods result in stronger stimulation of this centre after consumption? What element of food may be altered to help the obese reduce their dependence on these substances?

When we consider eating behaviour, several different parts of the brain are involved in the regulation of this important activity to our survival. An

Can Food Be Addictive?

interesting aspect, is that the part of our brain responsible for complex, conscious thought, does not have to function, for feeding activity to be retained. For example, babies born with severe brain injury to their cerebral hemispheres are still able to feed [1]. Rather, it is the mid brain that is responsible for automatic behaviour and motivation that is most involved in appetite and eating. One part is responsible for ensuring that we do not starve, and that we have enough energy to get by. This centre is the hypothalamus which detects the availability of ‘energy’, to ensure that our brains are adequately supplied with glucose. In animal studies, destruction of part of the hypothalamus is associated with failure to eat, and when other parts are destroyed, animals eat too much [1]. Scientists are now starting to explore the different brain circuits that underlie our eating behaviour. A distinction has been made between “homeostatic” and “hedonic” mechanisms of hunger, reflecting the different anatomical regions in the brain (Figure 1). While the hypothalamus seems to control our ‘need to eat’, because we have not eaten for some time and we’re running on reserves, the hedonic mechanisms, mediated by our reward centre, reflect the ‘want to eat’ [2]. Tied in with the ‘want’ can be ‘emotion’ and ‘liking’. The hedonic mechanisms are those linked with the addictive potential of food. The brain stem, along with the nerves in the nose, mouth and throat give information to the hypothalamus and reward centre about the food that is being consumed. Palatable food has an additional effect on the reward centre in the brain, promoting over eating which we will look at in detail in this chapter.

63


Figure 1. Simplified schematic of the machinery of the brain involved in appetite regulation. (Adapted from Erlanson et al, 2005)

These days very few of us live in an environment where we have to think hard about where our next meal will come from. In fact most people in developed countries eat on such a regular basis that we can never be short of energy. So, why do we over-eat?

To begin the discussion, we relate our own story of how we got invoIved in the idea of food addiction. Both of us began our research lives with little interest in food, in fact, we both were helping people stop smoking, and one of us (HM) is still largely associated with this area of study. The first evidence that we draw on to show that food shows characteristics of an addictive drug is that it seems to relieve withdrawal symptoms in smokers trying to quit.

FOOD ADDICTION: SIMILARITIES AND

INTERSECTIONS WITH TOBACCO DEPENDENCE

Addiction theory, relating to the reward centre in the brain, that we encountered in Chapter 2, is not only useful for researchers. The theory is intimately weaved into the strategies that help individuals quit smoking. We will briefly outline how this theory is applied to help people rid

64


themselves of their love affair with cigarettes. Smoking cessation counselling involves exploring with smokers the reasons that they smoke (mainly relief of withdrawal symptoms) and giving them some information about what symptoms to expect when they give up. During counseling, smokers are warned about the cues that prompt smoking, and how the use of slow release nicotine (patch and gum) can help them quench their withdrawal symptoms, acting as a bridge to liberty from nicotine dependence. Warnings of potential side effects of nicotine treatment (bad dreams from the nicotine patch being worn at night or nausea in the case of excessive nicotine) are given so that quitters don’t encounter unexpected surprises, and abandon their treatment. Behavioural techniques, such as “the four D's – delay, distract, drink water, and deep breathe”, are usually offerred to help with episodic craving, but research has failed to scientifically support their continued use. Most of the evidence for effective treatment consists of starting and maintaining individuals on slow release nicotine treatment.

Aside from the nuts and bolts of assisting people to quit, other knowledge about tobacco dependence intersects with food addiction. From our experience with clinical trials of novel nicotine products, we knew that time from contact with the addictive substance to experiencing reward was likely to predict the addictive potential of the drug, and as a result of their rapid nicotine delivery, cigarettes are highly addictive. The rewarding nature of smoking cigarettes is no accident; it is linked to the rapid absorption of nicotine in tobacco smoke by the small airways in the lungs, delivering nicotine to the smoker’s brain within seconds, although the maximal concentration when venous blood is sampled occurs at about 15 minutes after the first puff is inhaled. Cigarette companies are well aware of this, and they alter the acidity of tobacco so that nicotine in cigarette smoke is more rapidly absorbed by the lungs, yielding a quick “hit” or “kick” [3]. Cigarette companies have dressed up these changes, often effected by adding ammonium, as “flavour correction agents”, although the real intention is much more sinister. A survey of other common additives to cigarettes is revealing, as they are likely to have been added, in part to increase the rewarding nature of the smoke produced. Although marketed

65


as flavour enhancers, cigarettes are laced with sugar, licorice, chocolate and cocoa butter. The inclusion of these products are justified to improve taste, but as we will discuss later, these foodstuffs, themselves, are likely to have rewarding properties that acts with the nicotine, making the addiction harder to crack [4]. Although nicotine patches and gum contain the same addictive substance as cigarettes, the slower absorption, owing to the different method of delivery (across the lining of the mouth with gum, or across the skin from the patch) makes these products far less rewarding, or prone to long term use. Peculiar to nicotine is that, although in the form of cigarettes it is highly addictive, it does not cause serious adverse health effects. We are fairly certain about this last statement, because, over 30,000 patients have participated in clinical trials of nicotine products and no increased incidence of disease, hospital admission, or other events has been reported in the active treatment group over those that receive the inactive or dummy treatment (placebo) [5]. It is the tar, which accompanies the nicotine from a cigarette, that is most responsible for the links between smoking and all kinds of diseases.

Cigarettes, apart from their dramatic addictive potential, are also, the most widespread appetite suppressant available on the free market. While weight gain is a common side effect of giving up smoking, lesser appreciated is the effect that glucose and sucrose exert on craving and withdrawal symptoms during a quit attempt. Most smokers put on weight when they quit. In fact the average weight gain is around 5-8kg in the first year of abstinence [6]. The exact mechanism by which tobacco withdrawal results in such weight gain is not known. Various chemical brain messengers (neurotransmitters) have been implicated, but no definitive explanation has been forthcoming. At a simplistic level, one can appreciate that the lack of stimulation of the reward pathway in the brain after stopping smoking may be compensated by stimulating the centre with other substances or behaviours, such as eating. Interestingly, one recent explanation for the development of obesity is that such people are more likely to have an under-functioning reward system. So, one of the ways to compensate for the lack of reward is to overeat, similar to recent ex-smokers who are no longer stimulating their reward system with nicotine.

66


Weight that accumulates after quitting cigarettes is primarily an increase in body fat. Energy intake has been reported to increase by between 100 and 200 calories per day. Very often this excess energy comes in the form of sweet foods. I (HM) was speaking to a friend of mine, who stopped smoking some years ago, about this issue. To her this concept of needing to eat for reward after stopping smoking was so logical she wondered why I was discussing it tentatively as theory. She described eating sweet food (chocolate in particular) as something that made her ‘feel good’, similar to the way a cigarette would, taking away some of the withdrawal discomfort. Although the feeling was short-lived, for that moment, it made her feel normal again.

When delivering smoking cessation treatment, we normally advise people not to go hungry as evidence suggests that the risk of relapse back to cigarettes increases if quitters go hungry. For most, we advise to concentrate on first getting rid of cigarettes for at least a few months, then tackle the issue of the almost inevitable weight gain. If it is any consolation for people stopping smoking, the drugs they might use (such as nicotine replacement therapy or bupropion) can reduce post cessation weight gain, at least for as long as they are taken.

Smoking cessation researchers have been interested in this link between smoking and appetite for some time. As noted, restricting food intake whilst trying to stop smoking increases the risk of relapse and restricting energy intake increases cigarette consumption. Smoking acutely reduces hunger and in some studies has been found to decrease the desire for and consumption of sweet tasting food. In 1990 Robert West, a prominent smoking cessation researcher, often heard his patients describe their craving for cigarette as a hunger pang. This led him to wonder if hunger may become a cue for smoking and therefore alleviating hunger might help people stop smoking. One way to satisfy the need for carbohydrates and satiating appetite was to eat glucose. This prompted some randomised controlled trials that showed that glucose, compared to a placebo (aspartame, an artificial sweetener, was used most often), relieved urges to smoke and some other tobacco withdrawal symptoms. It also seemed to increase quit rates, although the effect was small when used on

67


its own [7]. From my (HM) own research on the use of glucose for helping smokers quit, the speed of glucose in reducing tobacco withdrawal symtoms (such as hunger and irritability) was within 10 to 15 minutes of putting the tablet in the quitter’s mouth. This is faster than most NRT products, with the exception of nicotine nasal spray. Finally, it seems that smokers need not worry about additional weight gain when using glucose. Findings showed no significant difference in post-cessation weight gain between participants on glucose and placebo.

Most of the research, to date, focussed on glucose, but some results suggest that sucrose (table sugar) may have a similar effect on withdrawal symptoms. So how is it working? It may be that glucose is simply relieving hunger. Given that sweet tasting placebo tablets were used in the studies, it is not just a matter of palatability. However glucose and other sugary items relieve tobacco withdrawal, such substances are likely to be at least one part of the puzzle that mediate food’s addictive properties.

Other Addictions

While our experience has been with nicotine, other drug-based treatment of addictions share the same principle to help addicts recover. Another well known example is heroin or cocaine, two powerful opium-like drugs commonly linked to abuse. Users often start by snorting the substance, which gives a moderately rapid hit, but later on opt for a more-rapid, intense hit, by injecting the drug. In recovery, health professionals often make use of the methadone, a drug from the opium class, with a much slower absorption and elimination rate, that may bridge the gap to either abstaining completely, or be used long term as an alternative to the more addictive, and less safe, street varieties. Such drugs partially relieve the unpleasant withdrawal symptoms associated with drug abstinence, and reduce the tolerance of the individual to the drug, by giving the user a slower, sustained hit. Although not described in the scientific literature, I have it on good authority, from people that work with opiate addicts, that in the early stages of abstinence, addicts tend to eat sugary food. Similar to

68


the relief that sugar and glucose bring to smokers going through withdrawal, we speculate that these carbohydrates also help quench the same symptoms in opiate users.

Could such knowledge help people with obesity and overweight, and solve the modern crisis afflicting developed nations the world over? Let us now look at more direct evidence that obesity is an addiction.

DOES FOOD HAVE ADDICTIVE POTENTIAL?

At first, it seems absurd to attribute addictive properties to food, a necessity of life we can not live without. However, the question of whether food fulfils the criteria for addiction, such as those laid out in the psychiatrist's bible, the DSM-IV, is really not the issue. What interests us is what effect different foods have on the “addiction” or “reward” centre in the brain, and which foods are likely to activate this centre most powerfully.

My (ST) interest in this area started when I flew from New Zealand to the United States to attend a conference about Nicotine and Tobacco. I was relatively new to the research world, and had never been to the United States before. I must say, I can not remember a single thing from all the talks, graphs, powerpoints, and earnest orations. What stood out to me was the food on offer. The conference organisers, situated in the Hilton Hotel, with distinguished attendees (me excepted), served a curious lunch for a New Zealander's palate. The meal consisted of a sandwich, with oddly sweet bread, two large plate-sized cookies and a packet of corn snacks, washed down with sweet orange juice. At that time, I hadn’t thought much about sugar. Being a cheapskate, figuring that I wouldn't be able to find better food readily available outside the Hilton confines, I persevered with what I considered an unusual meal for such a formal occasion. Mid way through the first biscuit, I noticed I was feeling nauseated, and couldn't continue. I thought that everyone in the conference must be feeling the same way. This food was too sweet, and wouldn’t be suitable for a children's birthday party, let alone an international academic conference.

69


Curiously, I looked around, observing other’s eating behaviour. Most people around me did not register a hint of discomfort, in fact they were hoeing into their second biscuit without hesitating. Some were even seeking a third. From my work helping smokers quit, I thought, this nausea could be excess stimulation of the reward centre, much like what occurs when a non-smoker first tries a cigarette. They tend to get a wave of nausea, until they persevere and develop some tolerance to nicotine. Was this same phenomenon happening to me with this insanely sugary, North American biscuit? I then faced the other conclusion, was this conference, populated with experts on the subject of nicotine addiction, a sample of the wider North American populace that were, themselves, addicted to sugar, or at least much more tolerant of the substance than I was? Other lights started to turn on. Was the public health messages I'd been hearing, blaming the food industry for large portion sizes, just a response to a more food, and sugar tolerant population? Was the growth in the size of soda bottles over the years, simply evidence of growing tolerance to sugar, rather than an industry-inspired plot? My curiosity was pricked and, I determined to press deeper.

Does sugar intake show evidence of addictive patterns of behaviour? Although by no means widely accepted in nutrition circles, both human and animal laboratory studies point in this direction. Of all the food groups, carbohydrate is commonly ascribed addictive properties, and within this category, sugar (sucrose). At a clinical level, in humans, carbohydrate craving has often been reported, although a full withdrawal syndrome has not yet been described. We portrayed one individual who recounted a likely food withdrawal syndrome following abstinence from sugar and white flour, which peaked after three days and resolved after one month of continued abstinence (described in detail later in the chapter). This pattern is similar to the temporality of symptoms observed in other addiction syndromes after abstinence (opiate or tobacco addiction). Anatomical changes found following sophisticated imaging, such as positron emission tomography, of people who suffer from drug addiction show evidence of adaptation, with increased concentration of dopamine receptors compared to controls. Such midbrain changes also occur in obese individuals. After

70


giving the short answer, we now recount how we became ‘accidental tourists’ in the nutrition field.

As I looked into definitions of addiction, I discovered that chemical addictions were described in language often reserved for food. In fact, what are addictions, other than a ‘hunger’ for drugs, or certain activities, such as gambling, the internet, or work? Ironically, in many books that I skimmed, describing addiction authoritatively, food got little more than a brief mention. In the realm of science, food addiction only seemed to be strongly grounded in the realm of neuroscience, where most of the subjects were rodents, with few human clinical studies attempted. Nutrition, as a whole, had almost completely ignored what I found to be an exciting new theory to explain the serious modern affliction of obesity and its many serious health consequences. Had we found the key to unlocking a hidden addiction? From an addiction point of view, the macro and micronutrients that seem to stimulate the reward pathways in the brain were pointing to carbohydrate, rather than fat – number one on the traditional ‘hit list’ of public health nutritionists. What do we know about the health effects of carbohydrates? Are all carbohydrates the same, or are there different forms? What I was most interested in, considering the addiction background, was “is there a slow release carbohydrate that might help us break this subtle addiction, similar to the nicotine patch available for smokers?”

During this time, I (ST) was pricked with curiosity about food. Since medical school, I had taken the received nutritional wisdom to heart and decided to abstain from fried food, eat minimal amounts of cheese, drink nothing but skim milk, and insisted on lean meat. I wasn't particularly over weight to start with, but my abdominal girth slowly but steadily expanded. Such adverse consequences only made me firmer in my resolve to continue with this Jack Sprat diet. One day I bought a cheap copy of Atkins book and was intrigued. The Atkins diet was popular with the public, however, the received medical wisdom suggested that eating such an energy dense diet of fat and protein should have the opposite effect of what was intended, and cause unfettered weight gain. In medical school, the Atkins diet had been labelled extreme, or a 'fad' diet, of no use to patients because

71


it clearly gave them the wrong message - eating fat was ok. Reading the book for the first time, I felt like a naughty boy, betraying the scientific integrity drummed into me consistently over the years. It was nutritional pornography. What I read, however, intrigued me. Atkins gave lucid descriptions of obese clients he had helped lose weight that described very clearly symptoms of a possible food withdrawal syndrome, similar to the tobacco withdrawal syndrome I had studied in smokers. One such patient recounted a sorry tale of unsuccessful trials of varied weight loss techniques such as laxatives, drugs that provoked vomiting and he even underwent surgery intended to effect weight loss. Nothing worked. He lamented:

“...often I would shake until I could put some sugar in my mouth.’’

Cues were also reported:

‘‘I had an hour’s drive from my office to my home, and I knew every restaurant, every candy machine and every soft drink dispenser along the whole route.’’

In more commonly accepted addictions, such as smoking cigarettes, those elements of the individual's environment that precede drug taking or reward become focal points of attention (cues) for substance users. In smokers, an example of cues include seeing other smokers light up, images of cigarettes or a pack of their favourite brand present in advertising or simply sniffing tobacco vapours in the air. Atkins’ description of his patient suggested that a similar syndrome occurred with his patient’s relationship with food. During his evening commute, the patient's attention was seemingly diverted, almost, against his will, in the direction of any likely source of food or sugar.

After making this discovery - that overeating and addiction shared many similarities - we wondered if others had made a similar discovery? What was the evidence for obesity being a hidden addiction? More importantly, how could we use this discovery to help people that were obese? One of the most effective treatments that help smokers quit, is slow

72


release nicotine from gum, or patch or other slow release nicotine containing product. The other question posed was what element of food is addictive? From other addictions, the most successful approach is to abstain completely from the most addictive forms of the substance. Such an approach is completely foreign to usual diets which advocate limiting the total energy from food, but not any particular food type. The question was what aspect of food is most rewarding, and most likely to promote overeating? We do not have all the answers to such questions, but we will recount our process of seeking responses.

We set out looking for a food equivalent of an indicator of the ‘time-to-hit’ from a cigarette. First, glycemic index caught our eye. Could this be the hidden key to unlocking the obesity problem? While working in a rather dull public health regulatory job, I (ST) and other colleagues penned an article, proposing that this might be the case. Briefly, we outlined that we, globally, were fatter than ever; that traditional nutition approaches to the obesity epidemic had done little to improve our collective predicament and that new ideas were needed. We proposed that the best predictor of the addictive potential of food was glycemic index, or glucose, because this index seemed the closest the nutritional world could offer that may parallel the time-to-hit seen with different nicotine products or cigarettes. We also summarised the evidence that linked eating behaviour with automatic thought and action, a characteristic of addictive behaviour. An interesting parallel we drew from addiction was the weight gain that accompanies smoking cessation, coupled with the knowledge that sugar, in the form of either glucose or sucrose, relieves craving for cigarettes, in smokers who are trying to quit. The first feedback I received about the article was from an emminent Professor of Public Health, who questioned what connection the theory had with the global obesity epidemic. In support of our hypothesis, we produced an article showing that global sugar consumption had risen more than 30% over the last thirty years. The article was ultimately printed in a little known medical journal. The next morning, I got a phone call from a UK journalist, who had stumbled over the paper. He seemed genuinely interested in the article and wrote a piece for the Daily Mail in the UK. Finally, the article was published some months later,

73


during the quiet news period over Christmas and New Year's Day in 2009. The headline was provocatively titled “Are you a carb addict?” and featured a crisp photo of a young girl about to tuck into an iced muffin [8]. What followed was the most extraordinary period of my life. I realised then that many in the press are sheep. Few lead, but many follow. The article was published in Norwegian, Hungarian, Italian, Romanian, and a number of other languages I couldn't identify from the internet. After a few days, the press in Australia interviewed me and the ensuing article appeared on the front page of the Sydney Morning Herald. The headline read “Revealed: why some foods are addictive”. This was a bit of an overstatement, considering that what we proposed was an idea - we hadn't proven anything, we had only put forward an idea. Nevertheless, many in the media claimed it as a fait accompli. Although the press coverage was gratifying on one level, it helped to sharpen my perspective on how public health policy, accepted wisdom, and scientific theories are propagated.

Initially, I thought the idea might attract some curiosity, at least. It was a new theory, proposing that glycemic index may be more important than previously thought, as a cause of global waist expansion. I thought the argument was reasonably argued, and not particularly controversial, after all, food addiction wasn’t a new idea, and we had only published the article in a journal entitled “Medical Hypotheses”, the article was very tentatively stated. We certainly didn't claim to have all the answers. It wasn’t long before we had our detractors. Possibly the world expert of glycemic index, Jennie Brand-Miller, a Professor of Human Nutrition at the University of Sydney, welcomed our theory, however, noted that glycemic index doesn't show a variable time-to-peak-concentration, unlike nicotine, that we had proposed. For cigarettes, the time-to-peak-nicotine-concentration is clearly much shorter for cigarettes than for nicotine gum or patch. We were grateful for the feedback, and began to correspond, by email. A potential flaw to the theory had been identified. At the same time, Professor Boyd Swinburn, a Professor of Public Health, then working at Deakin University, and consultant to the World Health Organisation on the subject of obesity, was the first to pour cold water on our idea. He showed that he wasn’t familiar with the word “addiction” by stating that obesity could not

74


be explained by an “addictive personality, or whatever”. Addiction research has long shown that drugs of abuse cause users to be hooked through development of tolerance and unpleasant withdrawal symptoms when the patient stops using the substance. While the personality of the user is important, it is not the principal mediator of addiction. The response was, however, revealing. I only realise now that the discipline of nutrition has almost completely overlooked the element of human motivation, and we had identified a gap in the dogma of nutrition experts. If eminent experts thought addiction had nothing to do with the cause of the obesity epidemic, who were we to question it? Swinburn rapidly dismissed our idea. What he didn’t realise was that the science of food addiction was decades old, with firm scientific foundations, and the controversial element of the paper was that glycemic index played a role in this addiction, much like that of nicotine playing a role as the addictive component of cigarettes. Suspicious of ‘experts’ before this event, this public dismissal cemented my resolve to uncover whether other apparent nutritional wisdom was not quite as ‘water-tight’ as it first appeared.

Despite little enthusiasm from one vocal expert critic, the public could relate to the idea. In fact a local news website put up a poll asking “Do you think carbohydrates are addictive”. Roughly 10,000 out of 15,000 respondents agreed. Also, e-mails flooded in from people who could identify with experiencing a withdrawal syndrome. One such respondent, from Wisconsin in the United States, reported:

‘For the first three weeks I cut all processed sugar and flour from my diet and suffered mood swings with extreme tension and depression, even a sense of hopelessness at times, I had horrible stomach pains, all my joints and muscles throbbed, and I had the shakes constantly. I don't even know how to describe the horrible headaches that went along with all this. People who knew me started thinking I was hiding a drug problem. The worst physical symptoms have been gone for about two weeks now, and the cravings are finally starting to subside… I look at birthday cake today and all I see is myself curled up in the foetal position crying in bed.

‘The worst part of the addiction lasted three weeks. The first three days were normal, but then on the fourth day the worst cravings began. All I could think about was ice cream, chocolate, and cheesecake. The cravings started to

75


subside after the third week, but once I started feeling better I [thought] about food less. The shakes and the headaches really were the worst part!’ [9]

With our familiarity with nicotine withdrawal symptoms, we were ready to pidgeon hole this correspondent’s description into this category. On closer inspection, however, the symptoms didn't quite fit. The woman described a number of different sensations after she stopped eating sugar and white flour, but most are not typical of tobacco, but opiate withdrawal. Body aches and pains are more commonly described after stopping heroin than cigarettes. The intense cravings she describes are, however, common to all withdrawal symptoms. Another interesting aspect of her history is the time course of the symptoms. A feature of nearly all addictions is the common time course of the symptoms. She recounts that the symptoms peaked in intensity after the first few days, and then started to subside after three weeks to a month. From alcohol to opiates to nicotine, withdrawal usually lasts between one to three months, with symptoms peaking in intensity over the first three days, and beginning to diminish markedly after one month.

After some correspondence, we cut and paste her response into a word processor, wrote a brief introduction and conclusion, and the piece was published in New Zealand's local medical journal. We felt that it was important to do so, because, incredibly enough, virtually no descriptions of withdrawal from food had been reported in either nutrition or medical journals. The tide of e-mails that we received after our paper hit the press suggests (at least to us) that this has been a gross oversight by the nutrition mainstream.

Aside from the Atkins' book, our ideas, and the e-mails, what evidence is there, in the established scientific wisdom that we searched, of food addiction? Do peer-reviewed, scientific publications offer any clues as to what aspects of food may be the key to unlocking the obesity epidemic? The result was yes, there is support, but mainly in the non-clinical, laboratory, rodent based studies. Despite a wealth of promising information in this area, few studies had spilled over from the laboratory to the clinic, and almost nothing into accepted nutrition dogma.

76


From chapter 2, we found that scientists had pinpointed a particular part of the brain, responsible for automatic behaviour, hunger for various drugs, and leads to the withdrawal and other features of addiction previously described (Figure 1). In obese people, we see that the same neural circuits, linked to addictive drugs, are also encountered in the physiology of appetite and hunger. Recently, specialised techniques have been developed to study how the brain responds to various stimuli (slow positron emission tomography (PET) studies). In one such study, eating stimulated nerve activity in the dopamine, reward pathway, known to mediate cocaine and nicotine addiction [10]. The same pleasure chemical (dopamine), which is stimulated by drugs of addiction, is also stimulated in people who are overweight. One characteristic of the brain, seen in substance abusers, and thought to be responsible for the tolerance that develops to addictive drugs is the reduced number of receptors that are activated by the release of this chemical into the microscopic space between neurons. Indeed, reduced dopamine (D2) receptor availability is strongly linked to increased fatness, indicating that increased dopamine levels are found in these regions of the brain. Such changes are likely to be the anatomical explanation for the increasing quantities of the substance often required to stimulate a similar dopaminergic (reward) response, due to reduction in receptor numbers. Low levels in this subtype of dopamine receptor have similarly been reported in people hooked on either cocaine, opiates and alcohol.

A small number of brain scientists have vigorously advocated that, on the basis of such findings, obesity should be categorised in a similar manner to other addiction syndromes. Despite such calls, little movement has occurred in the nutrition community. Perhaps the most vocal, Professor Nora Volkow, has summarised the similarities between the neural mechanisms underlying obesity and drug addiction, and even advocated that obesity be included as a specific subtype of addiction in the new ‘bible’ of psychiatric diagnosis - the Diagnostic and Statistical Manual (V) [11].

While obesity has yet to be classified as an addiction, some related eating disorders do appear in psychiatric texts. Binge eating is about as

77


close as the medical community has got to ‘food addiction’. The DSM, introduced in chapter two, is currently being updated (see www.dsm5.org). Within the eating disorders section is a proposed new diagnosis of binge eating. It has been defined as eating more than most people would eat in a discrete period of time and exhibiting a lack control during such sessions. To have a diagnosis of ‘binge eating disorder’ one has to

(1) recurrently binge eat, more so than just over eating at Christmas time, or at a birthday party (see number 4 below).

(2) binge eat with at least three of the following: eating more rapidly than normal; eating until you are so full you are uncomfortable; eating large amounts of food even though you’re not hungry; you eat alone because you’re embarrassed by how much you

eat; you feel guilty or disgusted with yourself afterwards

(3) feel distressed or worried about binge eating(4) binge eat, on average, at least once a week over a three month

period(5) Not compensate for binge eating (by vomiting afterwards, for

example) and the behavior is not associated with other eating disorders such as anorexia nervosa, bulimia nervosa or avoidant or restrictive food intake disorder.

Binge eating is usually specific for certain types of foods. For example, people don’t binge eat cabbage or carrots. So there is something more to binge eating than just eating large quantities of food.

Strong evidence highlights how eating behaviour is largely governed by subconscious, automatic thought processes. Such stereotyped actions are characteristic of drug addiction. Several mechanisms influence consumption that are not consciously controlled. This evidence comes from controlled experiments in which the external environment, rather than the individual, has a strong influence on how much food study subjects consume. In one study, increased portion size predicted greater food

78


intake, independent of body weight [12]. Also, ease of access to food increased consumption. For example, subjects consumed 5.6 more chocolates per day if the snacks were situated at their desk, rather than on a shelf, two metres away [13]. In another, subjects that were provided continuously refilled bowls of soup consumed 73% more soup than controls given non-filling bowls [14]. Such evidence suggests that the sight of food may stimulate over consumption by a Pavlovian stimulus-response, observed with other addictions. The importance of the food environment, tested here by measuring variation in food proximity, portion size and cues to eat, changed consumption behaviour in controlled conditions.

WHICH ELEMENT OF FOOD IS RESPONSIBLE FOR ADDICTION?

You may have noted that in the various case studies presented thus far, obese individuals that have experienced the characteristics of a withdrawal syndrome, such as the executive in Atkins’ book, or the woman who emailed us, described their symptoms as relieved by sugar, or were prompted by temporary or prolonged abstinence from sugar and/or white flour. In our survey of published scientific studies, both in the human and animal realms, evidence is also in favour of carbohydrates prompting reward over other nutrients.

Studies involving rodents have focused on carbohydrates as the most important elements involved in mediating addiction to food. In one study, rodents were trained to self administer glucose solution and data shows that such animals progressively increase their self administration with time [15]. A similar phenomenon occurs in response to sugar. Rats have been induced to have a sugar addiction syndrome, by feeding them high concentrations of the substance for about a month. Over this time, sugar intake generally slowly escalates over time, possibly indicative of tolerance to the food. The rats also tend to binge when the sugar solution first becomes available. This is a bit like the first cigarette of the day for a smoker. Using this model, scientists have also demonstrated that these

79


sugar binge eating sessions give rise to dopamine releases in the nucleus accumbens. This effect is similar to other drugs of dependence, although the magnitude is less than seen with morphine or cocaine, for example.

When rats are then deprived of sugar for 36 hours, they show signs of anxiety along with biochemical changes in the mid brain reward centre, typical of drug withdrawal. Opiate antagonists, such as naltrexone, reduces the severity of alcohol withdrawal and reduces craving after abstinence in sugar addicted rats [16]. Such a finding suggests that the opiate pathway is important in mediating sugar addiction, at least in rodents.

Our question of the comparative addictive potential of different major food types was investigated in one study, which compared rats fed a diet high in sugar and a diet high in fat. The rat withdrawal syndrome, that consists of eliciting various stereotyped tests for craving, anxiety along with physiological activation, only occurs in response to high sugar diets and not during or after exposure to high fat diets [15].

Have the addiction responses to different foods been studied in humans? Strangely enough, comparisons between different carbohydrates and comparing carbohydrate to fat or protein have been very rarely described. Despite the lack of comparative data, a number of descriptions of people with food withdrawal exist. Carbohydrate cravings have been recognized and reported to have higher frequency in subsets of patients with obesity related disorders, such as polycystic ovarian syndrome, and hormonal changes, such as premenstrual syndrome. Bonnie Spring, a professor of preventive medicine at Northwestern University in Chicago, found that a cohort of obese carbohydrate cravers recognized a carbohydrate rich drink and used it to relieve negative affective symptoms over an otherwise identical protein rich drink [17]. Also, refined carbohydrates have been shown to improve mood in a number of disorders such as seasonal affective disorder, severe premenstrual syndrome and overweight [18]. In this study in which protein and carbohydrate cravers were sought and compared, 70% of participants were carbohydrate cravers, with the majority (90%) female (compared to 53% male) [19].

80


Given the ubiquity of carbohydrates in modern western diets, obese people may not experience withdrawal symptoms from carbohydrates unless prolonged abstinence (>48 hours) is attempted. Instead the experience of obese individuals may be subtle symptoms similar to those of nicotine withdrawal, such as irritability, poor concentration, and urges that accompany short term abstinence from carbohydrate rich food. These subtle symptoms may be under-recognised as is the case in other addictions such as tobacco. Often, just the first hint of the onset of withdrawal prompts subconscious drives to perform the addictive behavior.

If glycemic index predicts the addictive potential of food we would expect that higher GI foods would produce earlier rewards in abstinent individuals than low GI foods, thus allowing Ainsley’s mechanism of delayed discounting to take effect, so that addicted individuals become selectively focused on foods that provide least delay in hedonic or rewarding effects. Such a study has investigated relief of hunger with a crossover design in young men of normal weight [20]. In this small study (number of subjects: 8 and 16), high glycemic index foods (glucose, polycose and sucrose) suppressed food intake one hour after consumption more than low GI foods (amylase and amylopectin). In another such study (12 subjects), liquid sucrose (table sugar) reduced hunger and produced greater satiety than fat (safflower oil) [21]. Also, increasing doses of sucrose resulted in reduced consumption of food post intake. Protein in contrast has been shown to suppress later food intake more than those foods that are high in carbohydrate and fat [22]. However, the meals used in the protein studies were not composed exclusively of one macronutrient, but rather had high proportions of fat, protein or carbohydrate. Given the interaction between high levels of fat and protein on glycemic index, such studies are difficult to interpret. These studies were also limited by small numbers, lack of blinding, and they involved normal weight subjects, so findings may not be applicable to obese subjects.

Experience travelling with a group from a Western country to China, in which average dietary sugar intake is much lower, also provides some insight into what are likely to be subtle withdrawal from refined carbohydrate. HM was on a 2-week vacation in China with thirteen of his

81


extended family from New Zealand. A good part of this trip involved being transported from one tourist site to the next, stopping only for main meals of the day and to use the bathroom at roadside service stations. The meals included in the tour package consisted of traditional Chinese fare. Starchy congee, noodles and eggs for breakfast with various combinations of meat, vegetables and rice for lunch and dinner. Hot, hot, hot! Notably absent was any dessert. The food was a novelty for the first few days, but it was only a matter of time before we all craved a sugary fix. At the regular toilet stops at service stations, we stocked up on chocolate and other sweets. We did not give our eating behaviour much thought, however, it did not go unnoticed by our tour guide who pointed out that sugar was best avoided in the traditional Chinese model of health.

Our initial theory related food addiction potential to the rate of absorption of glucose, expressed in the glycemic index. Support for this idea is drawn from parallels to the study of nicotine dependence and the effect of nicotine delivery devices on the blood and brain. Time to peak arterial concentration of nicotine predicts the addictive potential of a delivery device, with a cigarette providing the ultimate in fast delivery with peak concentrations delivered to the smoker’s central nervous system within seconds of inhaling [23]. Nicotine replacement therapy (nicotine gum, patch, inhalator or nasal spray), in contrast, has a slower profile, with the time-to-peak-concentration of nicotine gum between 30 and 60 minutes. The addictive potential of such products is lower, and so they provide a step, partially reducing nicotine withdrawal symptoms in recovering smokers, and roughly double the chance of quitting [5].

Glucose concentration after eating food, although demonstrating a similar profile to plasma nicotine after product use, does not exhibit the same changes in time to peak concentration, but instead rate of rise of plasma glucose concentration may be the key variable that predicts the addictive potential of food (Figure 1 contrasts studies of glycemic index and plasma nicotine). Fat and protein reduce glycemic index, by slowing the exit of food from the stomach. Time to peak blood concentration is thought to be most important in predicting the addictive potential of nicotine delivery products. Other properties of food may also have an

82


effect on the brain reward centres, such as fat, caffeine and various amino acids. Foods with other addictive agents may be more re-inforcing than predictions made from the GI alone, such as Coca-Cola®, which contains high levels of both sugar and caffeine.

(a)Source: Jennie Brand-Miller.

(b)Source: Royal College of Physicians.

Figure 1. (a) Contrasting plasma glucose profiles of a range of breakfast cereals (b) Contrasting plasma nicotine profiles of a range of nicotine delivery devices.

To explore the effect of taste, or palatability, let’s go back to our sugar addicted rats. You can test the influence of palatability (e.g. sweet taste) in

83


rats with a hole in their stomach (a gastric fistula). Here the poor rats can eat the sugar, and so experience the sweet taste, but it passes straight out of their stomach so that they don’t absorb any of the sugar. It was found that the sweet taste alone is enough to elicit dopamine release in the reward centre of the brain (the nucleus accumbens) [24]. This is somewhat different to the nicotine parallel, which emphasizes time to blood absorption as the essence of a product’s addictive potential. Clearly with food, taste also plays a major role, with the reward centre stimulated long before any nutrients are absorbed. The relative importance of nutrient absorption and taste on stimulation of the brain reward centre and addictive potential remains to be solved. Clearly, however, foods with a sweeter taste are likely to be more rewarding and addictive. Fructose, present in sucrose (table sugar) and high fructose corn syrup, is sweeter than free glucose. So it is likely that the extra sweet stimulation of taste buds from sugary food renders these foods more desirable than starchy counterparts.

A further clue to the addictive potential of foods comes from the use of drugs which switch off reward machinery in the brain. Opioid pathways (that mediate addiction to opiates such as morphine and heroin) appear to mediate the palatability and hedonic, or ‘want’ aspect of eating. In rats, a dose of naloxone which blocks opioid receptors in the brain, decreases intake of sucrose solution. Human studies also indicate that opioid pathways play a role in eating and reward. For example people maintained on methodone (stimulates receptors for opiods) report higher consumption of sweet food than those not using such drugs. More recently, a small flurry of studies on the use of naltrexone and bupropion for weight loss have appeared. Both of these agents are used in the treatment of addictions. Naltrexone, like naloxone, blocks opioid receptors in the central nervous system and in doing so reduces the ‘hit’ from opioid drug use. It therefore makes a useful treatment for people are addicted to such drugs. It is also used in treating alcohol dependence, where it is thought to help by blocking the effects of natural opioids (made in the brain) which are increased by excess alcohol intake. Bupropion is an atypical anti-depressant that interferes with the removal of dopamine and noradrenaline from reward centres in the brain. In the studies of bupropion use for

84


smoking cessation it was demonstrated that it not only doubled the subjects chances of quitting, but it also limited the amount of weight gained, compared to those who used a placebo. When naltrexone and bupropion are used alone neither of these drugs had a significant impact on weight loss. When combined, however, they exert a synergistic effect on appetite and weight gain [25].

SUMMING UP

From a variety of sources, including the treatment of people with addictions, anecdote, animal studies, and specialised human studies, evidence is accumulating that sugar and glucose containing food stimulates reward pathways in a similar way to that of addictive drugs. Although the strict clinical definition of addiction, described in the DSM, gives a picture of an individual totally obsessed and with a life ruined by their addictive substance, some similarities with other addictions are made. Less dramatic addictions, such as the prevalent need for regular coffee mid morning, may be a better comparator. Some consider the most important feature of addiction as the withdrawal syndrome, and we have some vivid accounts of such symptoms, prompted by a media story of our research. With this information, added to the drive to reduce fat consumption in the mid 60s, we may be reaching a point of putting some of the pieces of the obesity jigsaw puzzle together. Lower fat food, in general, means food richer in carbohydrates. Food rich in carbohydrates is then sensed by the brain as particularly palatable, driving increasing tolerance to the food, and trapping the individual to face unpleasant withdrawal symptoms if they try and cut down. Given that evidence of food addiction is starting to get a foot hold, let us explore how such information may help us tackle obesity for both individuals and populations.

85


REFERENCES

[1] Brobeck JR. Neural Control of Hunger, Appetite, and Satiety. Yale J Biol Med. 1957 Jun;29(6):565-574.

[2] Erlanson-Albertsson C. How Palatable Food Disrupts Appetite Regulation. Basic Clin Pharmacol Toxicol. 2005;97(2):61-73.

[3] Rose JE. Nicotine and nonnicotine factors in cigarette addiction. Psychopharmacology. 2005;184(3-4):274-285.

[4] Haustein KO, Groneberg D. Tobacco or health?: physiological and social damages caused by tobacco smoking. Springer Verlag; 2009.

[5] Silagy C, Lancaster T, Stead L, Mant D, Fowler G. Nicotine replacement therapy for smoking cessation. [see comment] [update of Cochrane Database Syst Rev. 2002;(4):CD000146; PMID: 12519537]. Cochrane Database of Systematic Reviews. 2004;3.

[6] McEwen A, Hajek P, McRobbie H, West R. Manual of smoking cessation: a guide for counsellors and practitioners. Wiley-Blackwell; 2006.

[7] West R, May S, McEwen A, McRobbie H, Hajek P, Vangeli E. A randomised trial of glucose tablets to aid smoking cessation. Psychopharmacology. 2009;207(4):631-635.

[8] Burne J. Are you a carb addict? 2009. [9] Thornley S, McRobbie H. Carbohydrate withdrawal: is recognition the

first step to recovery? New Zealand Medical Journal. 2009;122(1290):133-134.

[10] Wang GJ, Volkow ND, Logan J, Pappas NR, Wong CT, Zhu W, et al. Brain dopamine and obesity. Lancet. 2001;357(9253):354-7.

[11] Volkow ND, O’Brien CP. Issues for DSM-V: should obesity be included as a brain disorder? American Journal of Psychiatry. 2007;164(5):708-10.

[12] Diliberti N, Bordi PL, Conklin MT, Roe LS, Rolls BJ. Increased portion size leads to increased energy intake in a restaurant meal. Obesity Research. 2004;12(3):562-8.

86


[13] Wansink B, Painter JE, Lee YK. The office candy dish: proximity’s influence on estimated and actual consumption. International Journal of Obesity. 2006;30(5):871-5.

[14] Wansink B, Painter JE, North J. Bottomless bowls: why visual cues of portion size may influence intake. Obesity Research. 2005;13(1):93-100.

[15] Avena NM, Rada P, Hoebel BG. Sugar and Fat Bingeing Have Notable Differences in Addictive-like Behavior. J. Nutr. 2009;139(3):623-628.

[16] Grimm JW, Manaois M, Osincup D, Wells B, Buse C. Naloxone attenuates incubated sucrose craving in rats. Psychopharmacology. 2007;194(4):537-44.

[17] Spring B, Schneider K, Smith M, Kendzor D, Appelhans B, Hedeker D, et al. Abuse potential of carbohydrates for overweight carbohydrate cravers. Psychopharmacology. 2008;197(4):637-647.

[18] Christensen L, Pettijohn L. Mood and carbohydrate cravings. Appetite. 2001;36(2):137-45.

[19] Christensen L, Pettijohn L. Mood and carbohydrate cravings. Appetite. 2001;36(2):137-145.

[20] Anderson GH, Catherine NLA, Woodend DM, Wolever TMS. Inverse association between the effect of carbohydrates on blood glucose and subsequent short-term food intake in young men. Am J Clin Nutr. 2002;76(5):1023-1030.

[21] Woodend DM, Anderson GH. Effect of sucrose and safflower oil preloads on short term appetite and food intake of young men. Appetite. 2001;37(3):185-195.

[22] Anderson GH, Moore SE. Dietary Proteins in the Regulation of Food Intake and Body Weight in Humans. J. Nutr. 2004;134(4):974S-979.

[23] Schneider NG, Lunell E, Olmstead RE, Fagerstrom KO. Clinical pharmacokinetics of nasal nicotine delivery. A review and comparison to other nicotine systems. Clinical Pharmacokinetics. 1996;31(1):65-80.

87


[24] Hajnal A, Smith GP, Norgren R. Oral sucrose stimulation increases accumbens dopamine in the rat. American Journal of Physiology: Regulatory and Comparative Physiology. 2004;286(1):R31-37.

[25] Greenway FL, Fujioka K, Plodkowski RA, Mudaliar S, Guttadauria M, Erickson J, et al. Effect of naltrexone plus bupropion on weight loss in overweight and obese adults (COR-I): a multicentre, randomised, double-blind, placebo-controlled, phase 3 trial. The Lancet. 2010 Aug 21;376(9741):595-605.

88

Chapter 5

ADDICTED POPULATIONS:IMPLICATIONS FOR TREATMENT

When we speak about addiction to food, particularly to those with a scientific training, I'm often asked, “isn't it disempowering to obese people to label them with an addiction?”. We are not interested in labelling people as obese to condemn them, but to try and better understand why they struggle to lose weight and what can be achieved to set them on the path to recovery. Just as we have contrasted established addictions with eating behavior, we look now at how public policy has been recruited to get more smokers to quit and reduce uptake of the product. Could lessons from tobacco teach us how to slim national waistlines?

POPULATION LESSONS FROM TOBACCO

In Ian Gately's excellent book “La Diva Nicotina: How Nicotine Seduced the World” [1], the author describes how in the last chapter the scientific consensus was building that tobacco consumption caused lung cancer, and that in the 1960s, this was officially sealed in the US Surgeon General's report on Smoking and Health. Public health officials thought that these words would seal the end of smoking and thousands of people

would quit overnight once they were confronted with the truth of the risks they faced if they continued to puff. Unfortunately, this never happened. Most smokers that puffed before the Surgeon General put pen to paper, continued well after the ink had dried on the printing presses of his landmark opus. However the next thirty years were instructive for those trying to nudge population levels of smoking downward. Plenty of strategies were not effective. Number one was education. Teaching either adults or youths about the evils of smoking was not effective at reducing the uptake of the substance. Some strategies did, however, confer population benefits.

How was the population’s love affair with tobacco, or at least the nicotine in tobacco, eventually undone? Well, it is still very much an on going battle, but the most effective strategies so far have included limiting advertising, restricting sales to minors and hiking the price of cigarettes using tax increases. Such strategies aim to reframe tobacco use as unusual or abnormal, countering the effect of tobacco industry advertising. Following the revelation that ‘second-hand’ tobacco smoke was also harmful to one's health, many Western countries enforced smoking bans in public places, including bars, restaurants and work places. The state of New South Wales, Australia, even declared that smoking in a car with a youngster was a serious offence. Just as we have observed in the last chapter, in addictions, in which the behaviour is largely subconscious, or automatic, the ease of availability of the substance strongly influences consumption. Conversely, if, as a society, we are convinced that sugar is doing harm; then putting a cork on the fountain of sugar, using legislation and price rises with taxation is likely to be the most effective strategies to curb intake.

SUGAR AND TOBACCO?

Where does sugar stand in contrast to tobacco? Sugar, like tobacco was sixty years ago, is everywhere and is ubiquitous in the palates of diverse populations. Refined sugar has spread to virtually every corner of the

Addicted Populations: Implications for Treatment

globe. The principal proselytiser of sugar is the Coca-cola company, with their sugar heavy soft drinks universally recognised the world over. To eat sugar now is to do something which is perfectly normal, almost among any ethnic group, religion, or creed. In New Zealand, children are introduced to sugar at an early age. For most, sugary food is an everyday occurrence, along with sugary drinks and snacks. Appetites on hot days are often sated by ice-cream, a foodstuff that is usually more than 10% sugar. Most Westerners start the day with manufactured breakfast cereals, which are frequently between 20 and 40% sugar, by weight. Birthday parties, Christmases, Easter and Halloween all have sugary foods prominent on their menus. From food balance sheet data, held by the United Nations, it estimates that per capita intake of sugar in developed, English speaking countries, such as the United States, Australia, and the United Kingdom, is between thirty and forty teaspoons per day. In contrast, the most recent consensus statement from the American Heart Association (AHA) recommends restricting adults’ intake dramatically, to 9 teaspoons per day for men and 6 for women [1]. A 300ml can of coca-cola contains around 10 teaspoons of sugar –the daily allowance for men, and almost twice the daily allowance for women. The AHA did not report on the weighty implications of such advice in the context of a nation in which the average level of consumption is over four times higher than its upper limit. In the wake of the AHA’s statement, and the growing scientific consensus that fructose is a key component of the global obesity epidemic, little interest in restricting the sugar saturated diet of Western populations have surfaced.

In contrast to tobacco, however, alternatives are available to substitute for sugar. One of the most common sugary drinks on the market, “coca-cola”, has a zero sugar substitute. Artificial sweeteners such as aspartame are so sweet that only a small amount of the substance is required to flavour food products, and the total amount of calories consumed is negligible.

For tobacco, scientific consensus was an important step, marked by the publication of the Surgeon General’s report [2], linking smoking with a number of serious diseases (lung cancer, and heart disease). Although the Surgeon General has not produced such a document for sugar, the

91


recommendation by the influential, conservative, American Heart Association is a similar step. Little consensus exists, however, in Public Health Nutrition circles about the adverse health effects of sugar and fructose, and very few have taken a strong stance aimed at limiting the availability of sugar. Some public health activists have called for taxation on soft drinks, to discourage consumption of “empty calories”. We argue that sugar is likely to cause adverse effects not only as a result of its energy content. The fructose present in sugar is likely to, at a minimum, cause rotten teeth, and on the other extreme, contribute to the leading cause of premature death in most developed countries – coronary heart disease.

We argue that before action against sugar will progress, a substantial review of the health effects of sugar must be considered, to shape scientific consensus. What are the obstacles to progress leading to action aimed at giving sugar a similar status as tobacco, necessitating serious measures such as control of advertising and taxation? The first obstacles we encounter are competing nutritional ideas. For the last forty years, focus has centred on fat and energy density. The message to reduce fat to lower energy intake and reduce saturated fat (predominantly from animals) to lower the risk of coronary heart disease have been trumpeted long and loud by public health authorities. One of the leading organisations here at home, the New Zealand Heart Foundation solicits five simple steps to eating for a healthy heart: (1) eat plenty of fruits and vegetables; (2) if choosing meat, make it lean and include fish as an alternative; (3) choose low fat milk; (4) replace butter with margarines and healthy oils; and (5) reduce salt. Sugar is conspiculously missing (http://www.heartfoundation.org.nz).

We argue that these latter two directives – to reduce total fat and saturated fat – have a lesser role in improving either the health of populations or individuals than previously believed. We give several reasons that these messages are not only ineffective, but also dangerous. First, low fat foods, are often manufactured, and supplemented with sugar to reduce fat content. Second, intake of saturated fat, in large summaries of published data (known as meta-analyses), has not been linked with increased risk of coronary heart disease. Third, these messages have been essentially unchanged for the last thirty years, yet the rates of obesity in all

92


English speaking countries have increased substantially during this period. In short, these recommendations are derived from little evidence, and aside from likely doing no good, are likely to be causing major harm, by indirectly opening the flood gates to the manufacture of food with higher sugar content.

CHANGE REQUIRED?

We believe that major road works are required on the public health nutrition road if obesity is to be restrained. Which forces oppose such a change? Acute discomfort comes from acknowledging that perhaps some of our most treasured theories may have actually caused harm, rather than good. Inertia stands in the way of acknowledging that the weight of evidence has turned away from established views. Indeed, until recently, the American Diabetes Association were advocating that their patients consume more fructose, to control blood sugar levels. This advice has been retracted, however, due to concern for adverse effects of fructose on serum triglycerides, linked to coronary disease. The latest consensus statement from the American Diabetes Association is almost silent on the issue of fructose [3], although it is not recommended as a sweetening agent. Concern for fructose as a possible cause of the obesity epidemic has yet to enter the vocabulary of no more than a minority of those interested in public health research, let alone practice. However, just as we lament the lack of interest in the topic, the tide is beginning to turn in unsuspected quarters. Malaysia, faced with a shortage of sugar, with supply reduced from its importers, has turned the crisis to its advantage, seizing on the adverse health effects of sugar and urging its citizens to reduce intake to counter the onset of diabetes.

At present, much of the evidence for the adverse health effects of fructose rests on short term, moderate to high dose, randomised controlled crossover studies, that are small scale. Outcomes consist of either weight loss, or intermediate markers of disease, such as chemicals present in the blood, such as cholesterol, or uric acid. Long term evidence for sustained

93


weight loss, reduced diabetes risk, and other health benefits are needed to test whether these promising results translate in to long term gain. Whilst the evidence against fructose, in our minds, suggest the need for immediate action, others are only likely to be swayed by long term studies that demonstrate favourable results. Reduced incidence of diabetes, coronary disease and obesity, in patients randomized to undertaking long term, low fructose diets would constitute powerful, compelling evidence of benefit.

If consensus develops, that sugar and refined carbohydrates are addictive, this will add to the impetus for legislative controls, similar to those which govern tobacco sales, restricting price, advertising, and availability. What further evidence is needed to definitively show that sugar is addictive? We consider that the animal, along with the limited human studies, which demonstrate a withdrawal syndrome with sugar restriction, constitute adequate evidence that sugar addiction exists, if only in a minority of people. We do not know of any studies that have attempted to measure the extent, severity and time course of withdrawal symptoms in people who attempt to abstain from sugar and other refined carbohydrates. Further studies, in which obese people are recruited and asked to rate symptoms such as craving for sugar, appetite, ability to concentrate, restlessness, irritability, headache, and other potential withdrawal symptoms, may help provide further evidence of addiction. If sugar restriction does provoke stereotyped withdrawal symptoms, it does not mean that widespread population level controls should follow. Caffeine, for example, is widely accepted to foster addiction among those who consume its varied liquid forms, however, the lack of evidence of any harm associated with its intake, means that it is almost totally unregulated in most societies. The evidence of harm from sugar intake along with the addiction element promote the case for public policy change to limit dietary sugars.

From this position, action may be taken. We suggest a sugar tax, along with draconian and widespread limits on sales and marketing of sugary beverages and foods. Such actions are likely to be strongly resisted by the sugar and soft drink industries that have considerable muscle in influencing politicians and public opinion by advertising and political lobbying. We

94


also believe that doctors should counsel patients who are at risk of developing coronary disease to drastically reduce the level of sugar in their diets. High fructose intake is unequivocally linked to low levels of good cholesterol (HDL), high levels of triglycerides and rotten teeth. It is also likely to play a role in causing high blood pressure, high uric acid levels (that may lead to gout), weight gain and other diseases. Obesity plays a major role in a variety of common cancers. If primary care doctors can be convinced to strongly advocate for patients to reduce these substances, this is likely to also help bring political support for limits and swing public opinion.

Brownell summarised the arguments for introducing a soft drink (soda) tax to the United States. At the moment, in New Zealand and the US, diet and sugary soda have an equivalent price at the checkout. In his summary, Brownell proposed a one cent per ounce (30 mL) tax on sugar sweetened drinks, or taxing per gram of added sugar [4]. The effect of such a tax would be to make diet drinks cheaper and encourage consumers to switch to sugar free alternatives. Benefits of the scheme would include raising revenue for obesity research and strategies for improving nutrition, and improving health care for those who suffer from the consequences of overeating. This approach is similar to taxing other legal addictive substances that cause disease – such as tobacco and alcohol. Some people may view a tax on sugar sweetened beverages as regressive, punishing the poor who are least able to cope with price increases. Other negative views expressed that such a tax is a blunt instrument that will affect people not targeted, such as those that drink small amounts of such beverages.

Counter arguments may be made to such negative views, so that the tax may help poorer people save money, by choosing water over expensive soft drinks. Against the second objection, many examples exist of laws such as seat belt wearing, which target the many to improve the lot of just a few, and push the population distribution of risk in a particular direction. We argue that sugar shares many characteristics of other addictive substances, and that effective strategies that have been applied to control tobacco should be similarly exerted on sugar and refined carbohydrate. Currently, one of the barriers to such a policy is the confusion that reigns

95


among nutrition public health messages. Many campaigns, such as the National Heart Foundation of New Zealand, focus their activity on reducing the energy density of food, reducing saturated fat, and limiting salt content. Sugar hardly features. Here, deliberately, we have focused on the evidence that refined carbohydrates, sugar in particular, have on health. To our knowledge, little work has been done to apply Occam’s razor to the field of nutrition. The principle states that among competing hypotheses (such as the cause of obesity), the theory that makes the fewest assumptions is most likely correct. One study attempted such a prioritisation based on published evidence [5]. The authors ranked evidence for a number of nutrition exposures on the risk of study subjects developing cardiovascular disease, including the technique of meta-analysis, combining the results of many studies, into a single summary statistic. The Mediterranean diet and glycemic index were supported by the most convincing evidence, with saturated-fat-modifying diets near the bottom. Curiously, public health policy seems directed in the opposite direction, with saturated fat dominating many public documents discussing nutrition policy. Sugar, only recently raising scientific eyebrows as a potential cause of coronary disease, did not feature in the analysis.

Tax aside, what other strategies could be used to reduce the impact of sugar on society, and reduce addiction at a population level? If we look at the various attempts to reduce the harm from tobacco, a variety of measures have been taken. The World Health Organisation realised early on that tobacco consumption was a global issue, and co-ordinating efforts between countries was required. Price and taxation is one strand, with others including a variety of measures:

Protection from secondhand smoke; Regulation of the content of tobacco products; Packaging and labelling of tobacco products; Education, communication, training and public awareness; Tobacco advertising, promotion and sponsorship; Help to stop smoking

96


The convention also seeks restriction of sales to minors.Could any of these strategies be applied to sugar? Indeed many have

called for restriction of advertising of “junk food”, however, the definition of “junk food”, itself, is tenuous [6]. As we have discussed, the blanket statement by the American Heart Association, in the 1960s, which continues in the consciousness of the public, that limiting consumption of fat is desirable, points the finger squarely at fatty meals, such as hamburgers, fried chicken and chips. Indeed, taking this indictment at face value would put many Asian dishes, such as fried rice, or fried noodles in the “junk” category. As we have seen, the evidence that over indulgence in such foods leads to obesity is tenuous. Although sugary products, such as confectionery, soft drinks, chocolate and ice cream have also been included in the definition of “junk food”, the rationale for limiting such foods is not often given. Perhaps some form of intuition, or the traditional “empty calorie” [7] argument is relied upon. We argue that simply limiting the concentration of sugar in an item is likely to have the greatest effect to restrain waistlines, diabetes rates and the addictive potential of the individual foods. With the recent confusion and lack of evidence over what is considered “junk food” and harmful for the health of the populace, it is little wonder that action in the public policy realm to improve nutrition has hit the doldrums.

If one accepts the evidence for the addictive potential of sugar one can immediately see the conflict between the food industry and public health. Sugary food builds reliable, addicted consumers who develop a tolerance for more and more of the product on offer. To maximise profits, increasing the sugar content of one’s product must be a “no-brainer” for many in the food industry. Without the recognition that sugar is both addictive and carries long term, significant risks to an individual’s health, commercial interests will win over the meek voice of public health.

We are not proposing prohibition of sugar. However we are proposing measures that help people reduce their intake. What could a World Health Organisation devised ‘Framework convention on sugar control’ look like? Similarities to the tobacco version can be readily drawn. This book is an attempt at improving education on the subject, however, distributing the

97


evidence against sugar through state educational and health facilities may improve their dissemination. It amazes me that guidelines, written to help physicians prevent cardiovascular disease among at-risk patients, make no mention of sugar. Although the American Heart Association is sufficiently concerned about fructose to warrant advocating severe restriction in the diet, clinical prevention guidelines make no mention of the topic. In contrast, drug treatment, that carries risk of serious side effects (antihypertensives, cholesterol lowering agents, and aspirin) is widely recommended to people at risk of the disease. It is hard to believe that restricting sugar will lead to adverse effects, like those commonly associated with drug treatment.

The development of a consensus of the definition of junk food, adjudicated by the concentration of sugar, may improve restriction of the marketing of such products, particularly to those least likely to appreciate the long term health effects – children. The exposure of children to advertising raises important ethical issues. Children younger than 7 or 8 years have difficulty comprehending the persuasive power of advertising, instead considering them fun or entertainment. In Nordic countries, such as Sweden, targeting advertising to children, aged less than twelve years, is viewed as morally and ethically unacceptable, and is already banned by law. Belgium has similar advertising restrictions, however, other countries like Australia apply limits to preschoolers only, and the United States has very few controls on such commercial activity. With the recognition that sugar is harmful and addictive, the constant exposure of children to cues to eat, in advertising, is likely to stimulate intake, and such an argument may raise the impetus to legally restrict promotion. In 1997, in the US, advertising spent on sugary products accounted for vast sums, with breakfast cereals ($792 million), candy and gum ($765 million), soft drinks ($549 million) and snacks ($330 million) attracting the most capital [8]. Behind such expenditure are major commercial forces that will not support the dismantling of a major weapon in their quest for higher profits. We argue that focusing the message of public health nutrition on sugar, through legal means, is likely to have the greatest impact on reversing the rising tide of obesity. The current sporadic, disjointed approach to public

98


health nutrition can be easily exploited by those that seek to discredit the activity.

Nutrition labelling is another field of activity that has received some attention recently. Understandably, the focus of traditional nutrition has been on the energy and fat content. Various new strategies, aimed at simplifying the message have been offered, such as traffic lights, urging caution with some foods (“red”), moderation with others (“amber”), and encouragement to consume others (“green”). Again, thanks to the domination of the “energy density” ideology, confusion reigns. Focusing on sugar could simplify the information needed to convey to the consumer.

SUMMARY

With many varied interest groups advocating different strategies to improve population health, we are pessimistic about the possibility of introducing the phrase “sugar control” into modern public health practice. From the first chapter, in the most recent Oxford Textbook of Medicine, we saw evidence that the scientific and nutrition establishment has taken an opposite point of view to ours, stating that sugar is exonerated from causing significant harm to the health of the public. In contrast to sugar, “tobacco control” is a phrase that attracts immediate recognition in public health circles. From our standpoint, the evidence against sugar continues to develop daily, however, little attention is focused on removing the substance from the prominent place it occupies in modern diets. Experience with tobacco suggests that legal restriction of sales, advertising and price controls are likely to be most effective. Some progress has been made, however. The consensus of the American Heart Association and their strict limits on sugar intake, although it remains largely unnoticed, suggests that more doctors and researchers are beginning to take fructose seriously. The implications of this limit in a nation in which the average, per person consumption is 40 teaspoons per day, has scarcely been explored. Without major road works on the nutrition road, reprioritising sugar and refined carbohydrates as number one on the public health hit list,

99


we are unlikely to see a reduction in the burden of disease from overweight and obesity.

REFERENCES

[1] Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig RH, Sacks F, Steffen LM, Wylie-Rosett J, on behalf of the American Heart Association Nutrition Committee of the Council on Nutrition PA, Metabolism undefined the Council on EPrevention. Dietary Sugars Intake and Cardiovascular Health: A Scientific Statement From the American Heart Association. Circulation 2009;120(11):1011-1020.

[2] Center for Health Promotion and Education. Office on Smoking and Health. The Health Consequences of Smoking: Nicotine Addiction: A Report of the Surgeon General [Internet]. 1988; [cited 2011 Mar 24] Available from: http://profiles.nlm.nih.gov/NN/B/B/Z/D/

[3] Evidence-Based Nutrition Principles and Recommendations for the Treatment and Prevention of Diabetes and Related Complications. Diabetes Care 2003;26(90001):51S-61. [cited 2011 Mar 25]

[4] Brownell KD, Farley T, Willett WC, Popkin BM, Chaloupka FJ, Thompson JW, Ludwig DS. The Public Health and Economic Benefits of Taxing Sugar-Sweetened Beverages. N Engl J Med 2009;361(16):1599-1605. [cited 2011 Mar 25]

[5] Mente A, de Koning L, Shannon HS, Anand SS. A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Arch Intern Med 2009 Apr;169(7):659-669. [cited 2011 Feb 22]

[6] Handsley E, Mehta K, Coveney J, Nehmy C. Regulatory axes on food advertising to children on television. Australia and New Zealand Health Policy 2009;6(1):1. [cited 2011 Mar 14]

[7] Nestle M. Soft drink “pouring rights”: marketing empty calories to children. Public Health Reports 2000;115(4):308-19.

100


[8] Story M, French S. Food Advertising and Marketing Directed at Children and Adolescents in the US. International Journal of Behavioral Nutrition and Physical Activity 2004;1(1):3.

101

Chapter 6

CAN KNOWLEDGE OF FOOD ADDICTION HELP OBESE PEOPLE LOSE WEIGHT?

INTRODUCTION

So we've given a somewhat revisionist theory of why nations and individuals get fat, and what motivates them to eat. Can any of this science actually help in the real world, assisting obese people to lose weight? As addiction practitioners who have worked with smokers who want to quit, we believe that similar techniques can be adapted for people struggling with the battle of the bulge. How would such techniques differ from traditional diet strategies? If reward and motivation drive obesity and the obesity epidemic, why haven't strategies been developed before based on a framework of addiction? In this chapter we’ll explore how a model of addiction has been applied to eating behaviour, and how we would consider adapting techniques learnt to help people quit smoking to taking back control of their weight.

ALCOHOLICS ANONYMOUS FOR THE OBESE?

Surprisingly, treatment of food addiction has been carried out for many years, outside of a mainstream medical context. Overeaters Anonymous

(OA) is an organisation that uses an addiction model, similar to that of Alcoholics Anonymous, to support people that struggle with their relationship with food. Curiously, not all people who attend OA are overweight.

During the course of the research for this book, we spoke to a number of individuals who attend a local, New Zealand chapter of Overeaters Anonymous. The spokesperson that I interviewed was, contrary to my expectation, not obese at all. She was thin, petite and articulate. We met in her home, and she recounted some of her experiences with food and OA. She mentioned that in her teens and early twenties, she lost control of her eating. She would plan binge eating sessions, mostly consisting of sweet things, such as piles of cake, biscuits and other sugary baked goods. She would crave these sessions, meticulously planning the execution of the binge, often driving to and from the supermarket in such a frenzy of anticipation she would come close to crashing her car. She would then indulge, feel ill, guilty, worthless, finally vowing never to do such a thing again. Despite her resolve, the binges continued year after year, until they threatened her marriage and work. Through friends, she came into contact with OA, using the twelve steps to reorient her life to a journey toward physical, emotional and spiritual wholeness. The steps consist of a spiritual journey which mirrors those of the better known alcohol support group. Members are encouraged to admit their lack of power over food, seeing their pattern of eating as an illness rather than a personal failure, and that their lives have become dominated by eating. They then acknowledge a Power greater than themselves, that is able to restore sanity, and they turn their will over to Him (as individually understood). Faults and wrongs are confessed and commitment to the adherent’s Higher Power is then advocated, with the added task of sharing the same message with other people in need. Although my contact didn’t specifically mention the twelve steps, she was extremely grateful for the turn around she had achieved through the group, and the sense of control she now exerted over her eating, which translated into a happier personal and family life.

With the addiction question burning in my mind, I asked whether there was any specific element of food that she found would set off cravings for

Can Knowledge of Food Addiction Help Obese People ...

eating binges. “Sugar!”, she replied. She recounted that she continued to avoid all forms of sugar. Occasionally she would eat a takeout meal that would set off severe cravings she recognised that threatened to take her down the destructive path of binge eating. Thinking the meal didn’t contain sugar, on occasion, she had telephoned the eatery to verify the list of ingredients. Invariably sugar would be on the list.

Traditional dieting strategies have advocated counting energy intake, limiting overall food intake, but not any particular food. If any foods are discouraged, it is those that are energy dense, usually by virtue of their fat content. Hunting in the supermarket for low fat milk, low fat cheese, in fact low fat everything is supposed to lead to the path of leanness and weight control. Or does it? Long term evidence of effectiveness is surprisingly hard to find. For example, in a pooled study (meta-analysis) of weight loss among patients from twenty two studies with diabetes, the effect of a dieting intervention was 1.7kg weight loss (95% confidence interval 0.3 to 3.2) at the conclusion of studies which ranged from one to five years duration [1]. Such a modest weight loss underscores how difficult maintaining long term weight loss is, even among highly motivated individuals, based on traditional diets.

If we took an alternative view, that the most important element to achieving long term weight loss is to totally ignore the total quantity of energy passing through your mouth, but instead attempt to tame your desire, craving and urges to eat, what might such a treatment program look like? In medical settings, ignoring what we’ve discovered about overeater’s anonymous, what does treatment for addiction consist of? Complete abstinence to a particular drug is generally recommended, with attempts at cutting down often not a helpful strategy. As one quote from an individual so succinctly stated,

“When you are addicted to drugs you put the tiger in the cage to recover; when you are addicted to food you put the tiger in the cage, but take it out three times a day for a walk.”

Kerri-Lynn Murphy Kriz [1].

105


The parallels between smoking and eating are not complete, due to eating being a behaviour that cannot be put aside completely, such that the temptation to relapse, overeat and binge is ever present. Smoking cessation is simple in comparison. Although treatment has developed in complexity, the behaviour to avoid, smoking cigarettes, is simple. When we counsel smokers to quit, we advocate setting a quit day, and recommend total abstinence from cigarettes from that day forward. When individuals cut down, rather than quit, the few cigarettes they allow themselves to smoke during the day, take on added reward, given that the severity of withdrawal symptoms tends to be more intense, and so the relief after giving in to a smoke all the more sweet. It is almost as if traditional dietary techniques conform to this “cutting-down” approach, known to fail in the addiction setting. Complete abstinence to different food or nutrient types are not commonly advocated.

OUR ADVICE

Say that we were to accept the addiction model of obesity and overeating. How would treatment for weight management change? There are no easy answers here, as little has been formally evaluated, and we are largely extrapolating from experience with smokers. First, we would advocate identifying the addictive component of food, and planning continued abstinence to such a substance. This is difficult in the food setting, in which, we have identified concentrated fructose and refined glucose containing products as the main villains in food responsible for stimulation of the reward centre. An additional consideration would entail limiting foods that stimulate the reward centre quickly. Here soft drinks and fruit drinks stand out as high in quantities of fructose and glucose (outside of the US in the form of sucrose), and require little chewing effort and quick reward when consumed. The carbonation of soda drinks is also likely to increase the speed of absorption and add to the addictive potential of these beverages. It sounds obvious, but cutting out sugar from caffeinated drinks, such as tea and coffee is another potentially addictive source of sugar. Given the addictive properties of caffeine, the addition of

106


sugar, may make such drinks more rewarding and difficult to limit. Concentration of the addictive substance also contributes to its addictive potential. Foods such as breakfast cereals, sweets, cakes, iced bakery items, biscuits, cookies and ice cream stand out as further foods to avoid due to the concentration of sugar and glucose they contain. An easy way to check how much sugar is in manufactured food is to read the list of ingredients. The list is printed with larger contributors (by weight) first. If any of the words: “sugar”, “sucrose”, “evaporated cane syrup” or “high fructose corn syrup”, appear in the first five ingredients, we recommend leaving the product on the shelf. Dried fruit is also an important source of concentrated fructose. The nutrition facts panel can help. As a rough guide, we recommend eliminating all foods that are higher than 5% sugar. Some foods are sweetened, primarily, with glucose sugars that contain no fructose. We would recommend such products, sweetened with malt syrup, or glucose, over sugar containing alternatives.

We are undecided about the importance of glycemic index as a potential predictor of the addictive potential of a substance, given that it does not account for fructose. Sugar (sucrose) is most commonly described in animal studies of addiction, and in anecdotes of withdrawal symptoms, as the substance that brings relief. Glucose makes up half of the sugar molecule, and this substance, alone may also be addictive. Evidence for this comes in the relief that glucose tablets give to smokers trying to quit, described in chapter 4. Therefore, high glycemic index foods, such as white bread, and other items composed of high concentrations of white flour are likely to be useful to avoid. Substituting such foods with low glycemic index alternatives, such as whole grain bread may also reduce the stimulation of the reward centre. Replacing cooked potatoes, for whole grain foods such as lentils and chickpeas may also assist with weight loss. We refer the reader to www.glycemicindex.com for further information about this subject. While we believe that following recommendations based on glycemic index are useful when considering starchy foods, the paradigm assumes that fructose is not harmful. Therefore, we suggest ignoring the index (and advice from glycemic index advocates) when evaluating foods with a high fructose content. This includes all fruit, and

107

http://www.glycemicindex.com/


manufactured foods with a high sugar (or high fructose corn syrup) or honey content.

When treating patients recovering from tobacco addiction, warning them that they will feel a little miserable due to withdrawal, and counselling them through how to cope with these symptoms can be useful. Often, smokers are given behavioural techniques, or advised to use use nicotine gum to ward off potent cravings. Substituting high addictive potential carbohydrates, for those with lower addictive potential, may be one strategy. For example, using artificial sweeteners, such as aspartame (‘Nutrasweet’) in place of sugar, may reduce the craving for sweet products. Low carbohydrate snacks, such as nuts, cheese, or olives, may be another way to help reduce craving without giving in to the sugar fix. Giving obese people information of the likely time course, likely to be worse over the first few days, and improving over several weeks, may also help sure-up resolve among obese people to get through, knowing that the discomfort will be temporary. Because food withdrawal has only been partially characterised, we have little information about how frequently these symptoms occur when people restrict sugar and carbohydrate intake.

Another important element in the treatment of addiction is the supporting role of their environment, and the obese person’s immediate family and friends. Eliminating tempting sugary treats from the refrigerator, freezer and pantry make impulses to relapse into sugary binges more difficult to carry out. The cigarette equivalent is advising quitters to throw away all lighters, cigarettes, secret stashes, ash trays and smoking paraphernalia, to eliminate cues from the home. If the individual’s family pledges support for the obese person, by eliminating sugary food from the pantry, the risk of relapse is likely to be reduced.

Have low fructose diets been attempted in the real world? Ironically, most of the evidence against fructose has accumulated from dosing subjects up with fructose. Rats and humans have had their blood metabolic profiles deteriorated, blood pressure raised, waistlines expanded with high fructose diets, however, little published evidence exists to support the use of low fructose diets [2]. One study that supports our assertion of limiting fructose consumption is a randomised study of teenagers. If a large

108


proportion of fructose in the diet comes from sugar sweetened soft drinks, and such drinks are particularly addictive, then restricting use of such drinks may improve weight loss. Although the study is small, teenagers who consumed at least one caloric soft drink per day, aged 13 to 18 years were randomised to an intervention to replace their soft drinks with non-caloric alternatives or no intervention. Although, overall the difference between the groups at outcome was not statistically significant (not great enough to be exclude the possibility of a chance finding; -0.14 +/- 0.26 [standard error] kg/m2), the effect of the intervention was more exaggerated in youths who were overweight at study enrolment. If one considers only the third who were most overweight (by body mass index), the net decrease in body mass was unlikely to be due to chance, compared to the no intervention group (-0.75 +/-0.34 kg/m2). Observational studies, which are usually considered a weaker level of evidence than this randomised study, have also reported weight loss among a cohort of 810 adult subjects over 18 months of follow up, among those that reduced their sugar sweetened beverage intake. Change in other calorically sweetened beverages was not associated with weight change [3].

If limiting sugar is such a common sense, easy way of losing weight, why has it not been more widely championed or taken-up? A number of authors have written about the reducing fructose and their personal health improvement, as a result. The vocal critic of the Australian nutrition establishment, David Gillespie, published a recent book, entitled “Sweet Poison”, which has been influential in advancing the case against sugar. Richard Johnson, an American kidney doctor and researcher has published a similar book entitled “The Sugar Fix”, carrying a similar message, recommending low sugar diets. Johnson, however, does carry much of the tradition theories, whereas Gillespie has more vigorously rejected them.

109


Table 1. The sugar calculator

Food Description Sugar (teaspoons)

Soft drink Not diet drinks; per 330 mL can) 9

Powdered drink Per teaspoon added to water ...

Cordial Per 35g serve 4-5

Fruit juice Glass of orange or apple juice 4-5

Breakfast cereal or

muesli

with dried fruit or added sugar,

per 30 gram serve

4-10

Yogurt with added

sugar

200 ml tub 3

Table sugar added Added to tea, coffee, breakfast

cereal

...

Dried fruit Mini pack of sultanas 6

Chocolate or

sweets

Mars bar

Block of chocolate (125gm)

7

14

Honey or jam Per serve 2-4

Sauce (tomato,

BBQ, mayonnaise,

sweet chili)

Per serve 1-2

Dessert or ice

cream

Per 30g serve 2-4

Sweet biscuits Shortbread

Chocolate

Slice of cake

1

2

2

Alcohol

(fermented sugar)

10g standard drink (330ml beer or

90mL glass of wine)

3

Fruit Apple (125g; 1 cup)

Banana (225g; 1 cup)

Orange (180g; 1 cup)

3-4

7-8

5

Total __

Adapted courtesy of www.giveupsugar.com.

Aim for a maximum of 6 teaspoons per day for women and 9 teaspoons for men.

110


Recently, we published a paper in a local medical journal, with the title “The New Zealand sugar (fructose) fountain: time to turn the tide?” [4] to raise awareness of sugar and fructose intake in our home country, among the medical doctors. We had little response, initially, from anyone in New Zealand, however, I soon got a call from an anaesthetist from Melbourne, Australia, who was intrigued by our view point. Dr Rod Tayler, who worked mainly in private hospital settings had read, digested and become personally convinced of the book written by his countryman, David Gillespie. He was so persuaded of the low fructose approach, from personal experience, that he started running weight-loss discussion groups at the hospitals where he worked. His audience mainly consisted of female, middle-aged nurses, battling with body size, and looking for an answer to shed some excess fat. Rod’s message was simple, based on Gillespie’s book and the American Heart Association consensus, limiting sugar intake to no more than six teaspoons of sugar per day for women, and nine for men. The talk lifts the lid on how much sugar is present in commonly consumed foods. Conveying the message in simple measures (teaspoons of sugar), he encourages his audience to calculate their daily sugar intake using the sugar calculator he devised (Table 1). We have supplemented the table with quantities of sugar available from fruit, although we realise that the AHA guideline only applies to added, rather than intrinsic sugar present in fruit. The website may be viewed at www.giveupsugar.com.

He had such positive feedback from his audience, with stories of dramatic weight loss, that he continues to lecture and has expanded his client base to include cardiologists and other doctors. He is now evaluating the effects of the intervention using an observational study design. Rod came and visited me at my home in Auckland. From a brief read of his website, I noted an absence of material on addiction. I quizzed Rod about whether his audience reported cravings or major withdrawal symptoms in the early phases of embarking on his recommended diet? He had received a few reports, estimating that about 30% of people who attended his talk and followed his advice who then recounted suffering from cravings and withdrawal discomfort. Both he and I eagerly await the results of his study,

111


in which participants will be asked how they feel in the early stages of giving up sugar.

An important part of the puzzle provided by Rod was the focus on limiting the total quantity of sugar to a very low level, and appreciating the ubiquity of sugar, present in manufactured food. I was also staggered that an individual, immersed in anaesthesia, could develop an interest in an apparently unrelated area, spreading the message that had helped him control his appetite and waistline, in the face of an unsupportive mainstream nutrition environment. Rod has also demonstrated the importance of getting one’s hands dirty, testing the theory on real individuals, and learning from such experiences.

In our own efforts to cut down sugary food and refined carbohydrates, we noticed that our intake of fruit increased in the early stages. While fruit possesses less refined carbohydrate than processed foods, in large quantities, the sugar and reward obtained from fruit may undo some of the benefits from cutting down sugar from processed food. We suggest keeping an eye on fruit intake, particularly dehydrated varieties, in the early stages of coming off sugar. Rod noted that some participants in his give-up-sugar sessions did not lose weight until they cut-back on fruit.

SUMMARY

We suggest limiting both food and drinks high in sugar content and refined carbohydrates (foods high in free glucose) to beat sugar addiction. Abstinence is a traditional method, used to beat addiction to cigarettes and other drugs, very different from the cutting-down approach of traditional energy-based nutrition strategies. We advocate an abstinence approach to losing weight. Sugar, with its high concentration of fructose is bad for health and likely to lead to craving, tolerance and higher needs for sugar and greater hunger. Gaining control of one’s nutrition environment, eliminating sugary food and drinks from the pantry, replacing these with sugar free alternatives is, in our opinion, the most effective means to long term weight loss. Although the evidence suggests that such an approach is

112


likely to be effective, long term trials are not yet available to demonstrate its effect. We eagerly await the results of such studies.

REFERENCES

[1] Norris SL, Zhang X, Avenell A, Gregg E, Brown T, Schmid CH, et al. Long-term non-pharmacological weight loss interventions for adults with type 2 diabetes mellitus. In: The Cochrane Collaboration, Norris SL, editors. Cochrane Database of Systematic Reviews. Chichester, UK: John Wiley & Sons, Ltd; 2005 [cited 2011 Mar 10]. Available from: http://www2.cochrane.org/reviews/en/ab004095.html

[2] Tappy L, Lê K. Metabolic effects of fructose and the worldwide increase in obesity. Physiol. Rev. 2010;90(1):23-46.

[3] Chen L, Appel LJ, Loria C, Lin P, Champagne CM, Elmer PJ, et al. Reduction in consumption of sugar-sweetened beverages is associated with weight loss: the PREMIER trial. The American Journal of Clinical Nutrition. 2009 May 1;89(5):1299 -1306.

[4] Thornley S, McRobbie H, Jackson G. The New Zealand sugar (fructose) fountain: time to turn the tide? New Zealand Medical Journal. 2010;123(1311):58-64.

113

Health & Medicine

Sickly Sweet: electronic version